Matrine inhibits inflammatory response induced by TNF-α in human umbilical vein endothelial cells through miR-25-3p-mediated Klf4 pathway / 中国中药杂志

This study aimed to analyze the effect of matrine on tumor necrosis factor-α(TNF-α)-induced inflammatory response in human umbilical vein endothelial cells(HUVECs) and explore whether the underlying mechanism was related to the miR-25-3p-mediated Krüppel-like factor 4(Klf4) pathway. The HUVEC cell inflammation model was induced by TNF-α stimulation. After 24 or 48 hours of incubation with different concentrations of matrine(0.625, 1.25, and 2.5 mmol·L~(-1)), CCK-8 assay was used to detect cell proliferation. After treatment with 2.5 mmol·L~(-1) matrine for 48 h, the expression of TNF-α, interleukin-6(IL-6), interleukin-1β(IL-1β), and Klf4 mRNA and miR-25-3p was detected by real-time fluorescence-based quantitative PCR, and the protein expression of TNF-α, IL-6, IL-1β, and Klf4 was detected by Western blot. The anti-miR-25-3p was transfected into HUVECs, and the effect of anti-miR-25-3p on TNF-α-induced cell proliferation and inflammatory factors was detected by the above method. The cells were further transfected with miR-25-3p and incubated with matrine to detect the changes in proliferation and expression of related inflammatory factors, miR-25-3p, and Klf4. The targeting relationship between miR-25-3p and Klf4 was verified by bioinformatics analysis and dual luciferase reporter gene assay. The results displayed that matrine could inhibit TNF-α-induced HUVEC proliferation, decrease the mRNA and protein expression of TNF-α, IL-6, and IL-1β, increase the mRNA and protein expression of Klf4, and reduce the expression of miR-25-3p. Bioinformatics analysis showed that there were specific complementary binding sites between miR-25-3p and Klf4 sequences. Dual luciferase reporter gene assay confirmed that miR-25-3p negatively regulated Klf4 expression in HUVECs by targeting. The inhibition of miR-25-3p expression can reduce TNF-α-induced cell proliferation and mRNA and protein expression of TNF-α, IL-6, and IL-1β. MiR-25-3p overexpression could reverse the effect of matrine on TNF-α-induced cell proliferation and the mRNA and protein expression of TNF-α, IL-6, IL-1β, and Klf4. This study shows that matrine inhibits the inflammatory response induced by TNF-α in HUVECs through miR-25-3p-mediated Klf4 pathway.

Effect of Virtual Painless Ward Based on Mobile Internet on Pain Management for Patients after Craniotomy / 中国康复理论与实践

Objective:To evaluate the effect of virtual painless ward management based on mobile internet on pain management of patients after craniotomy. Methods:From May to October, 2019, 117 patients who accepted virtual painless ward management based on mobile Internet after craniotomy were selected as painless ward group. From December, 2018 to April, 2019, 117 patients previously hospitalized in the same department after craniotomy were selected as control group. The regression equation was established to compare the Numerical Rating Scale (NRS), nursing satisfaction and anxiety rate between two groups, and the general data, such as age, were taken as independent variables into the regression equation. Partial regression coefficient (B), odds ratio (OR) and 95% confidence interval (CI) of the painless ward management after adjustment compared with that of the non-painless ward management were calculated. Results:Multivariate regression analysis showed that, compared with the control group, the score of NRS within four days significantly decreased (B = -2.700, 95%CI -3.167 to -2.232, P < 0.001), the nursing satisfaction significantly increased (B = 0.542, 95%CI 0.289 to 0.795, P < 0.001), and the anxiety rate significantly decreased (B = -2.119, OR = 0.120, 95%CI 0.053 to 0.271, P < 0.001) in the painless ward group. However, the improvement of the anxiety rate might not completely depend on the decrease of NRS score (B = -0.112, OR = 0.894, 95%CI 0.727 to 1.100, P > 0.05). Conclusion:The procedure of virtual painless ward based on mobile internet could obviously improve the management level of analgesia for patients after craniotomy.

Oxymatrine alleviates oxidative stress in fat-induced insulin resistance mice by suppressing p38MAPK pathway / 中国中药杂志

This paper was aimed to investigate the effect of oxymatrine on fat-induced insulin resistance mice（IR）, and to explore the effects of oxymatrine on oxidative stress and on p38 mitogen activated protein kinase (p38MAPK) pathway. ApoE-/- mice with high fat diet for 16 weeks were selected as IR animal model and randomly divided into the model group, oxymatrine 25, 50, 100 mg•kg⁻¹ group. C57BL/6J mice were selected as the normal control group. Mice were gavage for 8 weeks. Fasting blood glucose (FBG), cholesterol (TC), triglyceride (TG), fatty acid (FFA) and serum insulin (FINS) in the plasma were detected. Activity of superoxide dismutase (SOD), glutathione peroxidase, glutathione peroxidase (GSH-Px) and content of malondialdehyde (MDA) in liver were detected. Reactive oxygen species (ROS) content in liver cells were detected by Flow cytometry. The expression of heme oxygenase-1(HO-1), γ-glutamyl cysteine synthetase (γ-GCS) of liver was examined by Real time PCR and Western blot. The protein expression of p38MAPK, p-p38MAPK was examined by Western blot. In the study, the authors found that oxymatrine reduced the levels of FBG, TC, TG and FFA, increased SOD and GSH-Px contents, decreased MDA and ROS content. Compared with model group, HO-1, γ-GCS mRNA and protein expression significantly increased in 50, 100 mg•kg⁻¹ oxymatrine group. The expression of p-p38MAPK decreased in oxymatrine group. The results showed that oxymatrine alleviate oxidative stress in hepatic by inhibiting the phosphorylation of p38MAPK, to ameliorate fat-induced insulin resistance mice.

Effect of Jinlida on changes in expression of skeletal muscle lipid transport enzymes in fat-induced insulin resistance ApoE -/- mice / 中国中药杂志

<p><b>OBJECTIVE</b>To study the effect of Jinlida on changes in expression of skeletal muscle lipid transport enzymes in fat-induced insulin resistance ApoE -/- mice.</p><p><b>METHOD</b>Eight male C57BL/6J mice were selected in the normal group (NF), 40 male ApoE -/- mice were fed for 16 weeks, divided into the model group (HF), the rosiglitazone group ( LGLT), the Jinlida low-dose group (JLDL), the Jinlida medium-dose group (JLDM), the Jinlida high-dose group (JLDH) and then orally given drugs for 8 weeks. The organization free fatty acids, BCA protein concentration determination methods were used to determine the skeletal muscle FFA content. The Real-time fluorescent quantitative reverse transcription PCR ( RT-PCR) and Western blot method were adopted to determine mRNA and protein expressions of mice fatty acids transposition enzyme (FAT/CD36), carnitine palm acyltransferase 1 (CPT1), peroxide proliferators-activated receptor α( PPAR α).</p><p><b>RESULT</b>Jinlida could decrease fasting blood glucose (FBG), cholesterol (TC), triglyceride (TG), free fatty acid (FFA) and fasting insulin (FIns) and raise insulin sensitive index (ISI) in mice to varying degrees. It could also up-regulate mRNA and protein expressions of CPT1 and PPARα, and down-regulate mRNA and protein levels of FAT/CD36.</p><p><b>CONCLUSION</b>Jinlida can improve fat-induced insulin resistance ApoE -/- in mice by adjusting the changes in expression of skeletal muscle lipid transport enzymes.</p>

Effects of Tongxinluo capsule on sciatic nerve apoptosis in spontaneous type II diabetic KK/Upj-Ay mice and mechanism research / 中国中药杂志

To investigate the effects of Tongxinluo capsule on sciatic nerve apoptosis in spontaneous type II diabetic KK/Upj-Ay mice, in order to explore its mechanism for improving diabetic peripheral neuropathy (DPN). KK/Upj-Ay mice were selected as the DPN animal model and randomly divided into the model, Tongxinluo low, middle and high group (1, 2, 4 g x kg(-1)). C57BL/6 mice were selected as the control group. Mice were given intragastrically for 12 weeks. Paw withdrawal latency, motor nerve conduction velocity (MNCV) and sensory nerve conduction velocity (SNCV) were detected. Apoptotic rate were detected by FCM. Bcl-2, Bax, Caspase-3 mRNA and protein expression in sciatic nerve were examined by Real-time PCR and Western blot. p38MAPK, p-p38MAPK expression were examined by Western blot. In this study,the authors found that Tongxinluo capsule could increase paw withdrawal latency, MNCV and SNCV. Apoptotic rate of sciatic, the expression of Bax and caspase-3 were lower, while Bcl-2 expression was higher in Tongxinluo group than those in model mice. The expression of p-p38MAPK significantly decreased in Tongxinluo group. The results showed that Tongxinluo capsule has protective effects on diabetic peripheral neuropathy of mice via inhibiting cell apoptosis and suppressing the expression of p-p38MAPK.

Protective effect of Qihuang Mingmu capsule on retina of diabetic mice and its impact on VEGF expression / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the protective effect of Qihuang Mingmu capsule (QHMM) on retina of diabetic mice and its impact on VEGF expression.</p><p><b>METHOD</b>Forty KK/Upj-Ay mice were randomly divided into the model group and high, middle and low dose QHMM (8.32, 4.16, 2.08 g x kg(-1)) groups. Additional 10 C57BL/6 mice were selected as the control group. Mice were orally administered for three months. Their general appearance, fasting blood-glucose (FBG) and glycosylated hemoglobin (HbA1c) were observed. Pathological changes of retina were observed by light microscope and electron microscope. The expressions of vascular endothelial growth factor (VEGF), growth factor receptors-1 (Flt-1) and growth factor receptors-2 (Flk-1) were examined by Real-time PCR (qPCR) and Western blot.</p><p><b>RESULT</b>QHMM could ameliorate the symptoms of diabetic mice to varying degrees, decrease FBG and HbA1c, alleviate pathological lesions of retina and decrease the expressions of VEGF, Flt-1, Flk-1 mRNA and protein.</p><p><b>CONCLUSION</b>QHMM has the protective effect on diabetic retinopathy of mice by inhibiting the expressions of VEGF, Flt-1 and Flk-1 and intervening VEGF-VEGFR signal transduction pathway.</p>

Clinicopathologic analyses of non-compaction of ventricular myocardium / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the clinicopathologic manifestations of non-compaction of ventricular myocardium (NVM).</p><p><b>METHODS</b>Clinical data, electrocardiograms, echocardiography images and pathologic changes were studied in five cases of non-compaction of ventricular myocardium.</p><p><b>RESULTS</b>The patient's ages ranged from 29 to 57 years old, all were males. Abnormal electrocardiograms were obtained in all of the 5 cases. Among them, 3 were diagnosed using echocardiography. Histopathologic examination showed that there were abnormally coarse muscle trabeculation and deep recesses, interlacing in arrangement, over the inner wall of the heart chambers. The compacted myocardium became thinning down gradually from the base to the apex of the heart. The non-compacted myocardium bundles locating close to the endocardium were coarse and orderless in arrangement, nuclei were irregular and abnormal, nevertheless, the arrangement and appearance of the muscle bundles near by the pericardium part were essentially normal and the cell nuclei were evenly distributed.</p><p><b>CONCLUSION</b>There are no specific clinical manifestations obtained in patients with non-compaction of ventricular myocardium, however, the pathologic changes are characteristic and a clinical diagnosis can be made by using echocardiography.</p>

Protective effect of Tongxinluo Ultramicro-pulverization on experimental myocardial infarction of rats / 中国中药杂志

<p><b>OBJECTIVE</b>To study the effects of Tongxinluo ultramicro-pulverization (TXLU) on experimental myocardial infarction and platelet aggregation of rats, investigate its mechanisms on ischemia heart disease and offer a reference to clinical usage.</p><p><b>METHOD</b>Rats were separated randomly into 7 groups: sham, model, diltiazem (0.15 mg x kg(-1)), TXL(1.2 g x kg(-1)), TXLU (1.2, 0.6, 0.3 g x kg(-1)). The experimental myocardial infarction was induced with ligating the left anterior descending branch of the coronary of rats. The infarction size was determined after myocardium tissue was stained with 2,3,5-triphenyltetrazolium chloride (TTC). And the serum of rats was separated to analyze CK, LDH, SOD, MDA. Another 60 rats were separated randomly into 6 groups: control, aspirin (0.15 mg x kg(-1)), TXL (1.2 g x kg(-1)), TXLU (1.2 ,0.6,0.3 g x kg(-1)). The rat platelet aggregation was induced with adenosine diphosphate (ADP) and collagen to observe the inhibitory effects of TXLU.</p><p><b>RESULT</b>TXLU could relieve the myocardial infarction size and weight stained with TTC significantly, the myocardial infarction size of the three groups of TXLU were (2.7 +/- 2.1)%, (3.4 +/- 1.2)%, (2.8 +/- 1.8)%, compared with model group (8.9 +/- 5.9)%, P < 0.05 or P < 0.01. The myocardial infarction weight of the three groups of TXLU were (8.4 +/- 3.5)%, (8.7 +/- 4.1)%, (9.7 +/- 4.1)%, compared with model group (l2.2 +/- 3.6)% P < 0.05 or P < 0. 01. And the content of MDA and the activities of CK and LDH in rats subjected with ligation of coronary artery were inhibited obviously too, compared with model group P < 0.05 or P < 0.01, then the activity of SOD increased. TXLU could inhibit the maximum percentage of rats platelet aggregation induced with ADP and collagen, the maximum percentage of platelet aggregation induced with ADP were (26.9 +/- 9.2)%, (24.4 +/- 13.4)%, (30.6 +/- 12.2)%, compared with control group (44.3 +/- 15. 7)% P < 0.05 or P < 0.01; The maximum percentage of platelet aggregation induced with collagen were (33.8 +/- 6.9)%, (32.1 +/- 8.3)%, (41.5 +/- 7.8)%, compared with control group (49.2 +/- 15.9)%, P < 0.05 or P < 0.01.</p><p><b>CONCLUSION</b>The experiment results indicated that TXLU could protect myocardial tissue of rats from ischemic injury and the mechanism may be related with antioxidation and inhibiting platelet aggregation, and the results also suggested TXLU could lower clinical dosage.</p>

Effects of the total flavone of radix puerariae on apoptotic cell and apoptotic related-gene in atherosclerotic plaques of apoE gene deficiency mice / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the anti atherosclerosis effect and related mechanisms of total flavone of radix puerariae (TFRP) on atherosclerotic plaques in apoE gene deficiency (apoE-/-) mice.</p><p><b>METHODS</b>apoE-/- mice were treated with saline, TFRP 15 mg . kg(-1). d(-1) or TFRP 85 mg . kg-1. d-1 (n = 8 each group) respectively per gavage for 12 weeks. The apoptotic cells in atherosclerotic plaques were then detected by TUNEL analysis, transmission electron microscope (TEM). The expression of CD-68, SMA and Caspase-3 were determined by immunochemical methods.</p><p><b>RESULTS</b>Early macrophage apoptosis signs were observed under TEM, TUNEL-positive and CD-68 positive cells were found in lipid cores of atherosclerotic plaques. TFRP significantly reduced the number of apoptotic cells in a dose-dependent manner [(0.38 +/- 0.17)%, (1.95 +/- 1.02)%, (10.50 +/- 5.89)%, respectively, P < 0.01] in atherosclerotic plaques. TFRP treatment also significantly reduced the immune expression of Caspase-3 protein in a dose-dependent manner.</p><p><b>CONCLUSION</b>TFRP significantly attenuated the development of advanced atherosclerotic plaques in a dose-dependent manner which might related to down-regulated expression of Caspase-3 protein and reduced macrophage apoptotic cells in atherosclerotic plaques post TFRP treatment.</p>

Effect of PMTG on atherosclerotic lesion formation and expression of ICAM-1 and VCAM-1 in ApoE-deficient mice / 中国中药杂志

<p><b>OBJECTIVE</b>To study the protecting effect of polygoni multiflori total glycosides (PMTG) on the atherosclerotic lesion formation and the expression of ICAM-1, VCAM-1 in aolipoprotein (apo) E-deficient transgenic mice.</p><p><b>METHOD</b>Thirty-two female apoE-deficienct mice were randomized into four groups: PMTG high dose group (150 mg x kg x d), low dose group (25 mg x kg x d), atorvastatin positive control group (5 mg x kg x d), and model group. At the end of the tenth week, all mice were killed. The serum levels of Total cholesterol (TC), Triglyceride (TG), High-density lipoprotein-cholesterol (LDL-C) were measured by enzyme dynamics method. Transmission electron microscopy (TEM) were used to observe the morphologic changes of aortic endothelia cell. The expressions of NF-kappaB were studied by SABC immunohistochemistry.</p><p><b>RESULT</b>As compared with the model control group. (1) PMTG could reduce the levels of serum TC, TG significantly (P < 0.01), and LDL-C level significantly (P < 0.01). (2) It could increase the levels of serum NO and the anti-oxidation capacities significantly (P < 0.01), but reduce the levels of serum MDA significantly (P < 0.01). (3) PMTG could keep the normal morphology of aortic endothelial cell. (4) PMTG could deregulated the expression of NF-kappaB in aortic wall.</p><p><b>CONCLUSION</b>PMTG could inhibit the occurrence and development of atherosclerotic lesions by its anti-oxidation abilities, which reduce LDL-C level. The low LDL-C level could deregulated the of expression of NF-kappaB, which could deregulated ICAM-1 and VCAM-1 in AopE-/-mice in aortic wall through.</p>

Effect of N(G)-nitro-L-arginine on inflammatory factor and neuronal apoptosis after focal cerebral ischemic injury in rats / 中国应用生理学杂志

<p><b>AIM</b>To evaluate the effect of NG-nitro-L-arginine (L-NA) on inflammatory factor and neuronal apoptosis after focal cerebral ischemic injury in rats and the possible mechanism of protective effect of L-NA against cerebral ischemic injury.</p><p><b>METHODS</b>Thirty male SD rats weighing 250-280 g were randomly divided into three groups (n=10): (1) Sham operated group (SH), (2) Ischemic group (IS), (3) L-NA group. In L-NA group L-NA 20 mg/kg was given intraperitoneally twice a day for 3 consecutive days. In IS group normal saline was given instead of L-NA. Focal cerebral ischemia was produced by middle cerebral artery occlusion (MCAO) for 12 h. A nylon thread with rounded tip which was inserted into left internal carotid artery cranially until resistance was felt. The distance from bifurcation of common carotid artery to the tip of the thread was about 18-19 mm. Focal cerebral ischemia was confirmed by left Horner's syndrome and right side hemiplegia. In SH group the carotid artery was exposed but no thread was inserted. The expression of TNF-alpha was determined by immunochemistry and the content of IL-1beta was measured by radio immunity. The Bcl-2 and Bax protein expression were detected by flow cytometry.</p><p><b>RESULTS</b>The expression of TNF-alpha and the content of IL-1 beta were markedly increased after MCAO. Significantly increased DNA fragmentation indication of apoptosis was detected after MCAO. The expression of TNF-alpha and the content of IL-1 beta was significantly lower in L-NA group than in IS group. The percentage of apoptosis cells and expression of Bax protein were markedly lower in L-NA group than in IS group but still significantly higher than in SH group. The expression of Bcl-2 protein was markedly higher in L-NA group than in IS group. There was no significant difference in the expression of Bcl-2 protein between IS and SH group.</p><p><b>CONCLUSION</b>L-NA could inhibit the increase in the expression of TNF-alpha and the content of IL-1beta, and protect neurons from apoptosis induced by focal cerebral ischemia through increasing the Bcl-2 protein expression and inhibiting the Bax protein expression.</p>

Effect of N(G)-nitro-L-arginine on mitochondria injury in focal cerebral ischemia rats / 中国应用生理学杂志

<p><b>AIM</b>To observe the effect of nonselective nitro oxide synthase inhibitor N(G)-nitro-L-arginine(L-NA) on mitochondria injury in focal cerebral ischemia rats.</p><p><b>METHODS</b>The rats were randomly divided into sham, ischemia and L-NA treatment group. The model of focal cerebral ischemia was prepared with thread embolism in rats. L-NA was administrated respectively at 2 h, 6 h, 12 h after middle cerebral artery occlusion (MCAO). Rats were killed and the mitochondria of cerebral tissue were isolated by differential centrifugation after L-NA treatment for 3 days. The swelling and the activity of mitochondria, and the activities of ATPase, SOD, GSH-Px in mitochondria and the contents of NO, MDA in mitochondria were measured. Ultrastructure changes of neuronal mitochondria were examined by electronic microscope in ischemia and L-NA treatment group.</p><p><b>RESULTS</b>The swelling of mitochondria was markedly increased and the activity of mitochondria was decreased, and the contents of mitochondria NO and MDA were markedly increased, the activity of ATPase, SOD and GSH-Px in mitochondria were decreased significantly after MCAO. Compared with ischemia group, the contents of NO were decreased after ischemia 2h, 6h, 12h administered by L-NA, and the swelling of mitochondria was decreased and the activity of mitochondria was increased, and the activities of ATPase, SOD, GSH-Px in mitochondria were enhanced and the contents of MDA in mitochondria were decreased after ischemia 12 h administered by L-NA. The neuronal cytoplasm and the mitochondria swelled, the cristae were disrupted, dissolved or disappeared in MCAO rats. Administration of L-NA could reduce these changes induced by cerebral ischemia in rats.</p><p><b>CONCLUSION</b>It could be concluded that L-NA could beneficially inhibit NO production. But it could't protect brain against damage in ischemia acute stage. It could improve mitochondria energy pump, ameliorate oxidative injury and increase the activities of mitochondria during postischemia, and then could effectively protect brain against damage induced by focal cerebral ischemia.</p>

The effects of polygoni multiflori total glycosides on the experimentally atherosclerotic formation in apoE-deficient mice / 中国中药杂志

<p><b>OBJECTIVE</b>To study the effect of polygoni multiflori total glycosides (PMTG) on the expressions of ICAM-1 and VCAM-1 in the apoE-deficienct (ApoE-/-)mice with experimental atherosclerosis (AS) and underlying mechanism.</p><p><b>METHOD</b>Thirty-two female apoE-deficienct mice were randomized into four groups: high dose PMTG group (150 mg x kg(-1) x d(-1)), low dose PMTG group (25 mg x kg(-1) x d(-1)), atorvastatin positive control group (5 mg x kg(-1) x d(-1)) and model group. At the end of the tenth week of treatment, all mice were killed. The serum levels of total cholesterol (TC), triglyceride(TG), high-density lipoprotein-cholesterol (HDL-C) were measured by enzyme dynamics method. Light microscopy were adopted to assess the degree of atherosclerotic plaque of aortic wall and image analysis was performed with computer. The expressions of ICAM-1 and VCAM-1 were studied by SABC imunohistochemistry.</p><p><b>RESULT</b>In comparison with the model group, (1) PMTG reduced the levels of serum TC and TG significantly (P < 0.01), but elevated HDL level obviously (P < 0.01) . (2) PMTG increased the levels of serum NO and the anti-oxidation capacities significantly (P < 0.05 and P < 0.01), but reduced the levels of serum MDA markedly (P < 0.01). (3) PMTG reduced also the extent of atherosclerotic plaque of aorta areas were (P < 0.05). (4) PMTG deregulated the expressions of ICAM-1 and VCAM-1 in aortic wall.</p><p><b>CONCLUSION</b>PMTG could inhibit the occurrence and development of atherosclerotic lesions by the regulating lipid metabolism and anti-oxidation and deregulating the of expressiona of ICAM-1 and VCAM-1 in AopE-/- mice in aortic wall.</p>

Rosiglitazone promotes atherosclerotic plaque stability in apolipoprotein e-knockout mice / 中华老年医学杂志

Objective To study the effect of rosiglitazone on plaque stability in ApoE-knockout mice. Methods Thirty-two 6-week-old ApoE knockout mice were used as atherosclerosis models in two groups: rosiglitazonegroup (n=18) and control group (n=14). Male and female mice were half separated into two groups. All mice were fed normal chow diet. Rosiglitazone group received rosiglitazone 17 mg/kg of body weight/day. The animals were sacrificed and aortae were prepared for analysis after fourteen weeks. Aortic root were cutted and prepared for paraffin section. The positive percentage of macrophage cells, smooth muscle cells, tumor necrosis factor-? and matrix metalloproteinase-9 in aortic lesions were measured by immunohistochemistry. The changes of grey gradient of collagen in lesion of both groups were measured by Masson stain. Results The positive percentage of smooth muscle cells [(38.5?7.2)%vs(18.6?6.7)%,P