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Objective:To study the effects of tetramethylpyrazine on the expressions of ferroptosis related molecules after spinal cord injury; To explore the mechanism of tetramethylpyrazine promoting the repair of spinal cord injury (SCI).Methods:Totally 36 SD rats were divided into sham-operation group, model group and tetramethylpyrazine group according to random number table method, with 12 rats in each group. The rats in the sham-operation group underwent laminectomy without injury to the spinal cord. The SCI model was prepared in the other two groups. The rats in the tetramethylpyrazine group were intraperitoneally injected with tetramethylpyrazine of 80 mg/kg, and the rats in the sham-operation group and model group were intraperitoneally injected with the same volume of normal saline, once a day, continuous intervention for 28 days. One day before operation and 1, 3, 5, 7, 14, 21, 28 days after operation, BBB limb motor function score was used to evaluate the limb motor function of rats. Nissl staining was used to observe the morphology of neurons. Prussian staining was used to observe iron deposition. Assay kit was used to detect the contents of MDA and ROS in spinal cord tissue. Western blot was used to detect the protein expressions of xCT, GPX4 and ACSL4, and qPCR was used to detect the mRNA expressions of mRNA of xCT, GPX4 and ACSL4.Results:On the 14th, 21st and 28th days after operation, compared with the model group, the BBB score of tetramethylpyrazine group increased ( P<0.01); tetramethylpyrazine could significantly improve the morphology and structure of neurons and reduce the iron content in spinal cord tissue; compared with the model group, the contents of MDA and ROS in the spinal cord tissue of tetramethylpyrazine group decreased ( P<0.01); the levels of xCT and GPX4 mRNA and protein increased ( P<0.01), while the expression of ACSL4 mRNA and protein decreased ( P<0.01). Conclusion:Tetramethylpyrazine can regulate lipid peroxidation by regulating the expressions of ferroptosis related molecules, which is conducive to the recovery of limb motor function in rats with spinal cord injury.
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Diabetic peripheral neuropathy （DPN） is a symptom and/or sign of peripheral nerve dysfunction that occurs in patients with diabetes mellitus when other causes are excluded. DPN， one of the most common complications of diabetes mellitus， can lead to disability， foot ulcers， and amputation at a later stage. Its pathogenesis is closely related to high glucose-induced inflammatory damage， oxidative stress， mitochondrial disorders， and apoptosis in neural tissues. The p38 mitogen-activated protein kinase （p38 MAPK） signaling pathway is a key mechanism mediating the expression of inflammatory factors， oxidative factors， and apoptotic factors of neural tissues in DPN. The inflammatory response， oxidative stress damage， and apoptosis， induced by the activation of p38 MAPK phosphorylation by factors such as high glucose， can cause cell lipid peroxidation， protein modification， and nucleic acid damage， which results in axonal degeneration and demyelination changes. The current treatment of DPN with western medicine has obvious shortcomings such as adverse effects and addictive tendencies. In recent years， the research on traditional Chinese medicine （TCM） in the prevention and treatment of DPN has gradually increased， and the exploration of Chinese medicine intervention in the p38 MAPK pathway transduction to improve DPN has advanced. The present study reviewed the relations of the p38 MAPK pathway with insulin resistance and peripheral neuropathy and summarized the molecular biological mechanisms involved in the pathological process of DPN， such as inflammation regulation， oxidative stress， polyol pathway regulation， and Schwann cell apoptosis in the past 10 years. In addition， the literature on Chinese medicine monomers， Chinese patent medicines， and Chinese medicine compounds in inhibiting inflammatory reactions， oxidative injury， and apoptosis of DPN peripheral nerves based on the p38 MAPK pathway， resisting axonal degeneration and demyelination changes， improving sensory and motor abnormalities， relieving peripheral pain sensitization， and facilitating nerve conduction mechanism to provide references for the development of new drugs for clinical prevention and treatment of DPN.
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ObjectiveTo explore the effect of Tangbikang granules （TBK） on sciatic nerve inflammation in diabetic rats through modulation of adenosine monophosphate-activated protein kinase （AMPK）/nuclear factor （NF）-κB pathway. MethodSD rats were fed with high-fat and high-sugar diet for 8 weeks and then treated with streptozotocin （STZ， ip） at 35 mg·kg-1 for modeling. Then the rats were randomized into diabetes group， low-dose （0.625 g·kg-1）， medium-dose （1.25 g·kg-1）， and high-dose （2.5 g·kg-1） TBK groups， and lipoic acid group （0.026 8 g·kg-1） according to body weight and blood glucose level， and a normal group was designed. After modeling， administration began and lasted 12 weeks. The body mass， blood glucose level， and thermal withdrawal latency （TWL） of the rats were detected before treatment and at the 4th， 8th， and 12th week of administration. At the 12th week， the sciatic nerve was collected for hematoxylin-eosin （HE） and Luxol fast blue （LFB） staining， and the structural changes of sciatic nerve were observed under scanning electron microscope. The levels of interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） in sciatic nerve were measured by enzyme-linked immunosorbent assay （ELISA）， and the levels of AMPK， phosphorylated （p）-AMPK， and NF-κB proteins in the sciatic nerve were measured by Western blot. ResultThe blood glucose concentration and TWL in the model group were higher than those in the normal group at each time point （P<0.01）. The levels of IL-1β， TNF-α， and NF-κB protein in sciatic nerve in the model group were higher than those in the normal group （P<0.01）， and the p-AMPK/AMPK ratio was smaller than that in the normal group （P<0.01）. Compared with the model group， TBK of the three doses lowered the TWL （P<0.05， P<0.01） and the levels of IL-1β， TNF-α， and NF-κB protein in sciatic nerve of rats （P<0.05， P<0.01）， and high-dose and medium-dose TBK raised p-AMPK/AMPK （P<0.05， P<0.01）. The sciatic nerve fibers were orderly and compact with alleviation of demyelination in rats treated with TBK compared with those in the model group. ConclusionTBK improves the function of sciatic nerve and alleviates neuroinflammation in diabetic rats. The mechanism is the likelihood that it up-regulates the expression of AMPK in the AMPK/NF-κB pathway and inhibits the expression of downstream NF-κB， thereby alleviating the neuroinflammation caused by high levels of inflammatory factors such as IL-1β and TNF-α due to NF-κB activation.
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ObjectiveTo explore the mechanism of Tangbikang granules （TBK） against diabetic peripheral neuropathy （DPN） based on network pharmacology and in-vivo experiment. MethodThe active components in medicinals of TBK and their target genes were searched from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）. The active components of the medicinals which are not included in TCMSP were searched from previous research. After the analysis of drug-likeness by SwissADME， the target genes of them were predicted with SwissTargetPrediction. DPN-related target genes were retrieved from GeneCards. The common targets of the disease and the prescription were the hub genes of TBK against DPN， which were uploaded to Metascape for Gene Ontology （GO） term enrichment and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis. High-sugar and high-fat diet and low-dose streptozotocin （STZ， ip） were employed to induce diabetes in rats， and then the model rats were respectively treated with low-dose （0.625 g·kg-1）， medium-dose （1.25 g·kg-1）， and high-dose （2.5 g·kg-1） TBK for 12 weeks. Sensory nerve conduction velocity （SNCV） was evaluated. After hematoxylin and eosin （HE） staining， the sciatic nerve was observed under light microscope to examine the nerve damage. Real-time PCR was performed to detect the gene expression of adenosine monophosphate-activated protein kinase （AMPK） pathway-related targets in rat sciatic nerve， and Western blot to measure the protein expression of AMPK and phosphorylated （p）-AMPK in rat sciatic nerve. ResultThe main active components of TBK， such as quercetin， kaempferol， β-sitosterol， leech pteridine A， stigmasterol， and baicalein were screened out， mainly acting on interleukin-6 （IL-6）， tumor necrosis factor （TNF）， protein kinase B （Akt）， JUN， and HSP90AA1 and signaling pathways such as AMPK， nuclear factor-κB （NF-κB）， and Janus kinase/signal transducer and activator of transcription （JAK/STAT）. Molecular docking results showed that β-sitosterol and stigmasterol had high binding affinity with IL-6， TNF， JUN， and HSP90AA1. As for the animal experiment， compared with the normal group， model group had low SNCV of sciatic nerve （P<0.01）， disordered and loose myelinated nerve fibers with axonotmesis and demyelinization， low mRNA expression of AMPKα， AMPKβ， peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）， Sirtuin 3 （SirT3）， mitochondrial transcription factor A （TFAM）， and low p-AMPK/AMPK ratio in sciatic nerve （P<0.05， P<0.01）. Compared with the model group， TBK of the three doses raised the SNCV （P<0.01）， restored nerve morphology and nerve compactness， and increased the mRNA expression of AMPKα， AMPKβ， PGC-1α， SirT3， and TFAM （P<0.05， P<0.01）. The ratio of p-AMPK/AMPK in the high-dose and medium-dose TBK groups was higher than that in the model group （P<0.01）， while the protein expression in the low-dose TBK group was insignificantly different from that in the model group. ConclusionTBK exerts therapeutic effect on DPN through multiple pathways and targets. The mechanism is that it activates and regulates AMPK/PGC-1α/SirT3 signaling， which lays a basis for further study of TBK in the treatment of DPN.
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ObjectiveThis study aims to investigate the therapeutic effect of Tangbikang granules（TBK） on type 2 diabetes mellitus （T2DM） complicated with non-alcoholic fatty liver disease （NAFLD） and to elucidate the underlying mechanism. MethodT2DM and NAFLD were induced in ZDF rats， which were then respectively treated （ig） with low-dose （0.625 g·kg-1）， medium-dose （1.25 g·kg-1）， and high-dose （2.5 g·kg-1） TBK for 12 weeks. Fasting blood glucose （FBG） and body mass were recorded every 4 weeks during the treatment. One week before sampling， the feed intake of rats was detected， and after 12 h night fasting， oral glucose tolerance test （OGTT） was performed. The area under the curve （AUC） was used to evaluate glucose tolerance， and the homeostatic model assessment for insulin resistance （HOMA-IR） was calculated. Blood in abdominal aorta and liver were collected for determination of blood glucose and lipid metabolism indexes： Fasting serum insulin （FINS）， serum total cholesterol （TC）， triglyceride （TG）， low density lipoprotein cholesterol （LDL-C）， high density lipoprotein cholesterol （HDL-C）， and nonesterified fatty acids （NEFA）. The liver was weighed to calculate the liver index， and the liver tissue morphology was observed and analyzed based on hematoxylin-eosin （HE） staining and periodic acid-Schiff （PAS） staining. The protein levels of insulin receptor substrate （IRS）， phosphatidylinositol 3-kinase （PI3K）， protein kinase B （Akt） and phosphorylated IRS and Akt were detected by Western blotting. All data were analyzed by SPSS 20.0. ResultThe feed intake of the model group was higher than that in the normal group （P<0.01）， and the feed intake the administration groups was lower than that in the model group （P<0.05， P<0.01）. At the 8th and 12th week， the body mass in the model group was lower than that in the normal group （P<0.01）. Compared with the model group， TBK reduced FBG in a concentration-dependent manner. The blood glucose level in OGTT and AUC in the model group were higher/larger than those in the normal group （P<0.01）. The blood glucose value in OGTT was decreased in TBK groups and the metformin group compared with that in the model group， and AUC in the administration groups was significantly different from that in the model group （P<0.01）. The serum level of FINS and HOMA-IR in the model group were higher than those in the normal group （P<0.01）， and they were lower in the TBK groups than in the model group （P<0.01）. Serum levels of TG， TC， HDL-C， NEFA （P<0.05， P<0.01）， and LDL-C were higher in the model group than in the normal group. Serum levels of TG， TC， LDL-C， and NEFA in the TBK groups were lower than those in the model group， and the levels of TG， LDL-C， and NEFA in TBK groups were concentration-dependent （lowest levels in high-dose TBK group）. Compared with the model group， high-dose TBK significantly increased the level of HDL-C （P<0.05）. Liver index of the model group was higher than that in the normal group （P<0.01）. The liver index of the administration groups showed a decreasing trend with no significant difference from that in the model group. As for the HE staining result of liver， the model group had unclear structure of liver lobule， enlarged cells of different sizes， and obvious steatosis of hepatocytes. TBK of all doses alleviated liver injury， particularly the high dose. For the PAS staining， compared with the normal group， the model group demonstrated significant fat vacuoles and significant reduction in purplish red glycogen granules in the cytoplasm. The staining results of high- and medium-dose groups of TBK were more similar to the normal group. Western blot was used to detect the protein expression of liver tissue. The expression of PI3K protein， p-IRS1/IRS1， and p-Akt/Akt in the model group were lower than those in the normal group （P<0.01）， and they were higher in the high-dose TBK group than in the model group （P<0.01）. ConclusionTBK exerts therapeutic effect on T2DM combined with NAFLD in ZDF rats by activating the typical PI3K signaling pathway.
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Objective:To observe the effect of Hippocampus kelloggi on GRP-78/PERK/ATF-4 signal pathway and explore its mechanism on improving spinal cord injury. Methods:A total of 36 SD rats were randomly divided into sham operation group, model group and hippocampus group with 12 rats in each group. Only laminectomy was performed in the sham operation group. The spinal cord injury model was prepared in the model group and hippocampus group. Rats in the hippocampus group were given 10 ml/kg Hippocampus kelloggi extract by gavage for 14 days. Basso Beattie Bresnahan (BBB) score was used to evaluate the motor function of the limbs. The neuron morphology was observed by Nissl staining. The expression of GRP-78, p-PERK and ATF-4 proteins were detected by Western blot, the expression of GRP-78 and ATF-4 mRNAs was detected by qPCR, Caspase-3 and Caspase-12 were detected by ELISA, and the apoptosis was detected by TUNEL. Results:Compared with the model group, the BBB score of hippocampal group increased on the 7th, 9th, 11th and 14th day after operation ( P<0.05). For hippocampus group, the relative expression of GRP-78 (0.49 ± 0.06 vs. 0.74 ± 0.03), p-PERK (0.63 ± 0.04 vs. 0.81 ± 0.06) and ATF-4 (0.51 ± 0.06 vs. 0.69 ± 0.05) protein were significantly decreased ( P<0.05), GRP-78 mRNA (0.54 ± 0.05 vs. 0.63 ± 0.06) and ATF-4 mRNA (0.61 ± 0.06 vs. 0.78 ± 0.04) were significantly decreased ( P<0.05), the content of Caspase-3 and caspase-12 were significantly decreased ( P<0.05), and the apoptosis rate of hippocampal group was significantly decreased ( P<0.05). Conclusion:Hippocampus kelloggi can regulate the stress response of the endoplasmic reticulum after spinal cord injury by inhibiting GRP-78/PERK/ATF-4 signaling pathway to promote the repair of neurons.
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This study was aimed to observe the effects of gymnema sylvestre total saponins (GA) on insulin resistance (IR) in adipose tissues of KKay mice,in order to discuss the action mechanism from the PI3K/AKT signal transduction pathway.A total of 27 KKay mice were randomly divided into the model group (DM),Pioglitazone group (BG) and GA group.Nine normal C57BL/6J mice were used as the normal control group (NC).Intragastric administration of drugs was given for eight weeks.The bodyweight and food intake of all mice were tested each week.After the experiment was completed,fasting plasma insulin (Fins) and fasting plasma glucose (FPG) were detected and the insulin sensitive index (ISI) was calculated.Expressions of PDK-1,AKT,P-AKT (Ser473),P-AKT (Thr308) in adipose tissues of epididymis in mice were detected.And expressions of PI3K-p85 mRNA,PTEN mRNA,APN mRNA were also measured.The results showed that compared with DM group,bodyweight of BG and GA groups were decreased (P＜0.05,P＜0.05);FPG and Fins level of BG and GA groups were decreased (P＜0.05,P＜0.05,P＜0.05,P＜0.05),ISI increased (P＜0.05,P＜0.05);APN mRNA increased in BG and GA group (P＜0.01,P＜0.01);PI3K-p85 mRNA increased in GA group (P＜0.05);P-AKT (Thr308) protein expression increased in BG and GA group (P＜0.05,P＜0.01);P-AKT (Ser473) protein expression increased in GA group (P＜0.05);the phosphorylation of AKT (Thr 308) was enhanced in BG and GA group (/9＜0.01,P＜ 0.01);the phosphorylation of AKT (Ser473) was enhanced in GA group (P＜0.01,P＜0.01).PDK-1 protein expression was decreased in BG and GA group (P＜0.05);PTEN mRNA decreased in BG and GA group (P＜0.05,P＜0.01).It was concluded that GA can ameliorate IR by sensitizing PI3κ/AKT signal pathway in adipose tissues of KKAy mice.
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BACKGROUND:Rat models of complete spinal cord transection are common models for neural tissue engineering. After transecting the spinal cord by the previous methods, gap length of broken end cannot keep relatively uniform, so we cannot objectively evaluate effects of various treatments or tissue engineering materials. OBJECTIVE:The spinal cord transection models were established by using double edged micro scissors, andthe feasibility of this new model was explored by comparing with the conventional method. METHODS: A total of 42 adult female Sprague-Dawley rats were divided randomly into group A (n=6), group B (n=18) and group C (n=18). Group A only received laminectomy. In the group B, the spinal cord was transected with a sharp-pointed knife. Knife point should touch anterior wal of spinal canal and sidewal bone surface. Complete spinal cord transection models were prepared by repeated cutting. In group C, complete spinal cord transection models were established by using self-made double edged micro scissors. RESULTS AND CONCLUSION: (1) At 1 week after model establishment, in the groups B and C, complete paralysis of the hind limbs was found, and BBB scores were similar. However, significant differences in the spacing of broken end were detected. (2) At 4 weeks after model establishment, hind limb functions could restore to different degrees in both groups, but no significant difference in BBB scores was found. (3) At 8 weeks after model establishment, significant differences in hindlimb motor function scores were detectable between both groups. Biotin glucosamine tracer display: In group B, a few labeled axon fibers were observed at the caudal side of the injured spinal cord. In group C, spinal cord was completely transected, and labeled axon fibers cannot be found at the caudal side. (4) Results suggested that the modeling method of self-made double edged micro scissors could effectively eliminate individual differences, contribute to quantitative analysis and comparative study of therapeutic effects.
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BACKGROUND:Chinese medicineTangbikang can improve nerve conduction velocity in diabetic rats, and has anti-inflammatory and antioxidant effects. Insulin like growth factor-I is a key target in the treatment of diabetic peripheral neuropathy. OBJECTIVE:To observe the effect ofTangbikangon the expression of insulin-like growth factor-I and its receptor protein and mRNA in the sciatic nerve of diabetic rat model. METHODS:The experimental diabetes melitus rat models were induced by feeding high fat forage and injection with streptozotocin. After model establishment, rats were givenTangbikang 4.18, 8.35, 16.7 mg/kg per day. This study set positive control methycobal, model and normal control groups. Intragastric administration was performed for 16 weeks. RESULTS AND CONCLUSION: Compared with the model group, blood glucose levels were similar in the methycobal group, but decreased in the high-doseTangbikang group (P < 0.01). Immunohistochemical staining and real-time fluorescence quantitative PCR detection revealed that body mass, motor nerve conduction velocity, insulin like growth factor-I and its receptor protein and mRNA expressions were increased in the methycobal and high-dose Tangbikang groups (P< 0.05 orP < 0.01). Results indicated that Tangbikang can prevent and treat diabetic peripheral neuropathy by promoting insulin like growth factor-I and its receptor. Cite this article:Mu XH, Sun W, Qin LL, Wu LL, Li WL, Guo X, Zhang L, Liu TH.Effects of Tangbikang on insulin like growth factor-I and its receptor expression in sciatic nerves of diabetic rats. Zhongguo Zuzhi
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This study was aimed to investigate the action mechanism ofHypoxis Hemerocallidea (African Potato, AP) on the AMPK signal pathway of skeletal muscles in diabetic rats. Among 40 male SD rats, 10 rats were used as the normal group, and the other 30 rats were fed with high-fat food for one month, and then injected with STZ for the model establishment. After the successful model establishment, rats were divided into the model group, pioglitazone hydrochloride group and the AP group. Intragastric administration was given for 5 weeks in each group. Then, the skeletal muscle tissues were embedded and sliced for immunohistochemistry test. The protein expression of p-AMPKα, p-AS16 and GLUT4 in skeletal muscles was detected by western blot. The 100 mmol·L-1 glucose was used in the establishment of C2C12 skeletal muscle cells insulin resistance model. AP drug-containing serum was used in the establishment of the treatment group. The control group was the normal cells. Glucose consumption, cell proliferation, SOD content, and MDA content were detected. And the protein expressions of p-AMPKα, p-AS160, GLUT4 were detected with the western blot and RT-PCR. The results showed that compared with the normal group, AP can up-regulate p-AMPKa protein express (P < 0.01), increase skeletal AS160 phosphorylation level (P < 0.01), and up-regulate the GLUT4 level (P < 0.01). Compared with the normal group, the high glucose caused the decrease of C2C12 skeletal muscle cell activity and the decrease of glucose consumption (P < 0.05), decrease of SOD, increase of MDA (P < 0.01), and the decrease of p-AMPKα, p-AS160, GLUT4 protein expression (P < 0.01). After 48 h intervention, the SOD of C2C12 skeletal muscle cells in the AP drug-containing serum group was significantly increased (P < 0.01), the MDA content was decreased (P < 0.05), the AMPKa and AS160 phosphorylation levels were increased (P < 0.01), the GLUT protein expression was increased (P < 0.01). It was concluded that the induced AMPKa and AS160 phosphorylation promoted GLUT 4 expression may be one of the action mechanism of insulin resistance of skeletal muscles in diabetes.
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This study was aimed to observe the effect ofGuava leaf total flavonoids on HIT-T15 pancreaticβcell insulin resistance. Effective part of FSL was prepared. The dosing time, concentration and high glucose concentration of FSL were confirmed by observing HIT-T15 pancreaticβ cell growth curve and the influences of HIT-T15 pancreaticβ cell proliferation by different concentrations of glucose and FSL. Afterwards, the influence of FSL on HIT-T15 pancreaticβ cell insulin secretion, the expression of insulin receptor mRNA and insulin receptor substrate (IRS) 1 protein were measured under the environment of high glucose. The results showed that 50 mmol·L-1 glucose can significantly inhibit the proliferation of HIT-T15 pancreaticβ cell (P < 0.01). The 50μg·mL-1 FSL can significantly promote the proliferation of HIT-T15 pancreaticβ cells (P < 0.01), the insulin secretion (P < 0.05), the expression of insulin receptor mRNA (P < 0.05), and the protein expression of IRS 1 (P <0.01). It was concluded thatGuava leaf total flavonoids can promote the insulin secretion of HIT-T15 pancreaticβ cells under the circumstance of high concentration of glucose which may be related to its effect of increasing expression of insulin receptor mRNA and IRS-1 protein.
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BACKGROUND:Titanium artificial cervical disc has good biocompatibility, but titanium al oy is shown to have poor biological activity, low bonding strength, easy release of metal ions under physiological conditions. OBJECTIVE:To observe the effects of different coating for the titanium plate of domestic cervical artificial disc on adhesion and differentiation ability of rat bone marrow mesenchymal stem cel s. METHODS:Passage 3 bone marrow mesenchymal stem cel s from Wistar rats were seeded into 24-wel titanium plates with hydroxyapatite coating, titanium powder+hydroxyapatite coating and bare titanium plate. Cel culture was terminated after 24 and 48 hours, and the cel growth was observed under scanning electron microscope. After 24 hours of inoculation, osteogenic inducer was added;then, cel supernatant was col ected at 3, 5, 7 days after cel lysis and centrifugation to detect the activity of alkaline phosphatase. RESULTS AND CONCLUSION:After composite culture with titanium plates with hydroxyapatite coating or titanium powder+hydroxyapatite coating, cultured cel s were in polygonal shape, and pseudopodia were extended into the micropores that were adhered closely to the material surface. Cel s cultured with bare titanium plates had poor differentiation and adhesion rate. With time, the expression of alkaline phosphatase was increased in each group, especial y in the groups of titanium plates with hydroxyapatite coating and titanium powder+hydroxyapatite coating (P<0.05). These findings indicate that titanium plates with hydroxyapatite coating or titanium powder+hydroxyapatite coating can promote adhesion and differentiation of rat bone marrow mesenchymal stem cel s.
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This study was aimed to explore the effect of Tang-Nai-Kang (TNK) on trans-differentiation of renal tubular epithelial cell in KKAy mice in order to discuss the possible mechanism. Fifty 12-week-old male KKAy mice were randomly divided into the model group, valsartan group, TNK high-dose, middle-dose and low-dose group, with 10 rats in each group. Ten C57BL/6J mice were used in the normal group. Rats in the model group and normal group were given 0.9% sodium chloride solution. Rats in other groups were given the corresponding drugs. After 8 weeks of gavage administration, kidneys of all mice were sampled and given Mosson and PAS dyeing. Expression distribution of α-smooth muscle actin (α-SMA) and E-cadherin in kidney tissues were observed under immunohistochemical staining. Expression of transforming growth factor-β1 (TGF-β1) was measured by western blot. The results showed that compared with the normal group, the area of renal fibrosis in the model group was significantly increased (P < 0.01); the expression of α-SMA was stronger; and the expression of E-cadherin was weaker. Compared with the model group, the area of renal fibrosis in the valsartan group, TNK high-dose, middle-dose and low-dose groups were significantly decreased (P< 0.01); the expression of α-SMA was weaker (P< 0.01);and the expression of E-cadherin was obviously increased (P < 0.05). The TGF-β1 expression in the model group was significantly higher than that in the normal group (P < 0.01). Compared with the model group, the TGF-β1 expression in the valsartan group, TNK low-dose, middle-dose and high-dose groups were significantly lowered (P<0.01). And the TGF-β1 expression in the TNK high-dose group was even lower than that in the valsartan group. It was concluded that TNK was able to suppress the epithelial-mesenchymal transition (EMT) of renal tubular epithelial cell, and lessen the renal tubule interstitial fibrosis, in order to protect the kidney.
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This article was aimed to study effects and mechanisms of Gymnema sylvestre on protein kinase B (PKB) and its phosphorylation in adipose tissues of KKAy mice which were mainly characterized by insulin resistance (IR). A total of 18 KKAy mice were randomly divided into the diabetes model (DM) group and Gymnema sylvestre (GS) group according to body weight levels. And 9 normal C57BL/6J mice were used as the normal control (NC) group. Intragastric administration of medication was given to mice for 8 weeks. At the end of the experiment, all animals were tested for fasting plasma glucose (FPG) and fasting insulin level (Fins) for evaluation of insulin sensitivity index (ISI). Expressions of phosphoinositide-dependent kinase-1 (PDK1), PKB, P-PKB (Ser473), P-PKB (Thr 308) in adi-pose tissues of epididymis were determined. The expression of phosphatase and tensin homolog (PTEN) mRNA was also determined. The results showed that compared with the DM group, the GS group showed lower FPG and Fins, higher ISI. The expression of P-PKB (Ser473) phosphorylation and P-PKB (Thr 308) were increased, and the PDK1 and PTEN mRNA were decreased. It was concluded that GS can improve insulin sensitivity of KKAy mice through activating PKB by up-regulate the expression of P- PKB (Ser473) and its phosphorylation ratio and P- PKB (Thr 308) in adipose tissues.
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@#Objective To explore the effect of enhanced physical therapy with integrated traditional and western medicine on muscularweakness after selective posterior rhizotomy. Methods 44 children with muscular weakness after selective posterior rhizotomy were dividedinto the treatment group (n=28) and the control group (n=16). Exercise therapy, physical therapy, electroacupuncture and Chinese massagewere applied to the treatment group, while exercise therapy was applied to the control group only. The muscle strength of the leg of childrenwere compared right after the surgery and 2 weeks after the surgery. Results The muscle strength of the leg of children in treatment group recoveredbetter than the control group 2 weeks after the surgery (P<0.05), and it was almost at the same level with that before surgery (P<0.05). Conclusion The enhanced physical therapy with integrated traditional and western medicine method could rapidly recover the musclestrength of the leg of children after SPR.
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BACKGROUND: Tension headache means contraction headache or oppressive headache in bilateral occipital-cervical part or whole head. Its pathogenesy bas not been completely known yet, which may be related to many factors and the conventional therapy is drug heteropathy but the effects are different, especially on patients with chronic disease and side effects will be induced by long-time intake of drugs.OBJECTIVE: To explore the curative effect of oral negative pressure on patients with tension headache and its mechanism of ameliorating microcirculation disturbance.DESIGN: Case-control observation.SETTING: Department of Pathophysiology of Hebei North University.PARTICIPANTS: Twenty patients with tension headache in the Department of Neurology, First Affiliated Hospital of Hebei North University from December 2001 to June 2002 including 12 females and 8 males,aged 18-28 (mean 23.4) with the disease course of 1-6 years, were randomly divided into therapeutic group and control group with 10 patients in each group.METHODS: The oral negative pressure instrument was applied. Put the negative pressure exerting equipment in the optimal position of mouth, adjusted the negative pressure to (0.05±0.01) MPa. The therapeutic time was 10 minutes each time (5 minutes for the first time) once a day with the time fixed. There were 5 days in one course and totally 3 courses. Put the negative pressure exerting equipment into mouth of patients in the control group for 10 minutes each time without exerting negative pressure. Quantitative evaluation on pain was performed with visual analogue scale (VAS)method, excellent as the VAS score decreased above 70%, effective as the VAS score decreased between 30% and 70%, invalid as the VAS score decreased below 30%. XTL- Ⅱ type microcirculation micro-television system was used to observe the changes of nailfold microcirculation by magnifing 260 times. The first row nailfold of left ring figure was checked conventionally, state of microvessel, micro-bloodstream and peri-loop were recorded and degree of microcirculatory disturbance was quantitatively analyzed according to TianNiu 's weighing integral method.MAIN OUTCOME MEASURES: The therapeutic effect after three courses and results of microcirculation observation.RESULTS: Totally 20 included patients were involved in the analysis of results. VAS scores of 7 patients in the therapeutic group decreased above 70% (70%), while no patient in the control group; VAS scores of 2 patients in the therapeutic group decreased from 70% to 30% (20%) and one patient in the control group (10%); VAS scores of one patient in therapeutic group decreased below 30% (10%) and nine patie nts in the control group (90%). Negative pressure could obviously ameliorate the microcirculation disturbance and enable it to recover from moderate before treatment to nearly normal with the total score decreased from (4.18±0.68) points to (1.97±0.41) points (P ＜ 0.01).CONCLUSION:Oral negative pressure has a significant curative effect on patients with tension headache. Its mechanism may relate to the improvement of microcirculation and the adjustment of nervous functional disturbance.
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BACKGROUND: Microcirculation disturbance of pharynx may be one of the pathogenesis base caused recurrent attacks of chronic pharyngitis. The negative pressure can improve the microcirculation of inflammary target organs by biomechanical changes.OBJECTIVE: To explore the therapeutic effect of oral negative pressure on patients with chronic pharyngitis and nail fold microcirculation.DESIGN: A randomized single blind controlled observation.SETTING: Department of Pathophysiology of Hebei North University.PARTICIPANTS: A total of 65 patients with chronic pharyngitis and course of disease about 1-3 years admitted to Department of Neurology,First affiliated Hospital of Hebei North University from January to September 2002 were selected. They were randomly divided into treatment group (n=35) and control group (n=30), including 36 cases with chronic pharyngitis (18 cases from the treatment group, 18 cases from the control group), 29with chronic hypertrophied pharyngitis (17 cases from the treatment group,12 cases from the control group).METHODS: The Hices oral negative pressure instrument was used and the negative pressure exert equipment was put into the optimal position of the patients' mouth to keep the negative pressure of (0.05±0.01) Mpa, 10minutes once (the first therapy time was 5 minutes), once daily and the time was fixed, 5 days as a period of therapy for three periods. Patients in the control group were also given the negative pressure exerts equipment,but no negative pressure was exerted.MAIN OUTCOME MEASURES: ① Observation and evaluation of nail fold microcirculation: The nail fold microcirculation was observed by the XTL- Ⅱ microcirculation micro-television system, and the first row nail fold of the left ring figure was checked conventionally to record the state of microvessel, state of micro-bloodstream and peri-loop. The degree of microcirculatory disturbance was quantitatively analyzed according to Tian Niu's weighing integral method, the lower the scores, the better the microcirculation. ②The improvement of chronic pharyngitis after treatment of 3courses.RESULTS: Totally 65 patients with chronic pharyngitis entered the stage of result analysis. ①After 1 course of treatment, the symptoms of 1/3 of the patients in the treatment group were significantly improved; after 3 courses of treatment, except there was no obvious changes of hypertrophied morphology such as lymphatic follicle proliferation on posterior wall of throat and hypertrophy on side cable of throat, the pathological signs and prevalence of mucosa congestion were obviously lower than those before treatment and the control group (P ＜ 0.05-0.01) effective rate was 88.6%.②) Improvement of microcirculation disturbance with chronic pharyngitis was evident, restoring to basically normal from medium degree abnormality before treatment, the total score values reduced to 1.941 ±0.165 from 4.836±0.242 (P ＜ 0.01).CONCLUSION: Oral negative pressure can significantly release or eliminate the symptoms and signs of chronic pharyngitis, which may relate to improvement of microcirculation disturbance.