Relationship between the Height of Alveolar Bone Resorption and Sex and Age in Adolescents / 法医学杂志

OBJECTIVES@#To explore the relationship between the height of alveolar bone resorption and sex and age in the adolescent dentition.@*METHODS@#Multi-slice computed tomography (MSCT) was used to measure the height of alveolar bone resorption at labial, lingual, mesial and distal sites of teeth in 149 adolescents aged from 10 to 20 years. SPSS 25.0 software was used to analyze the relationship between the height of alveolar bone resorption and sex and age.@*RESULTS@#There was no significant difference in the height of alveolar bone resorption between sex (P>0.05). The height of alveolar bone resorption was positively correlated with age in all types of teeth. The model constructed by combining the alveolar bone resorption height data of four sites (y=2.569x1+3.106x2+4.108x3+1.451x4-0.082, R2max=0.756)had a better ability to infer age than that of combining two sites (y=5.942x1+4.489x2+0.612, R2max=0.706) and a single site (R2max=0.638).@*CONCLUSIONS@#The height of alveolar bone resorption is positively correlated with the age of adolescents. The combination of four sites has a stronger ability to infer the relationship between the height of alveolar bone resorption and age in adolescents and has higher accuracy in practical application.

Regulatory Effect of General Anesthetics on Activity of Potassium Channels / 神经科学通报·英文版

General anesthesia is an unconscious state induced by anesthetics for surgery. The molecular targets and cellular mechanisms of general anesthetics in the mammalian nervous system have been investigated during past decades. In recent years, K channels have been identified as important targets of both volatile and intravenous anesthetics. This review covers achievements that have been made both on the regulatory effect of general anesthetics on the activity of K channels and their underlying mechanisms. Advances in research on the modulation of K channels by general anesthetics are summarized and categorized according to four large K channel families based on their amino-acid sequence homology. In addition, research achievements on the roles of K channels in general anesthesia in vivo, especially with regard to studies using mice with K channel knockout, are particularly emphasized.

Influences of Gender and Age on the Prevalence and Complications of Nonalcoholic Fatty Liver Disease / 中国医学科学院学报

Objective To investigate the effects of gender and age on the prevalence and complications of nonalcoholic fatty liver disease(NAFLD). Methods A total of 8429 NAFLD patients were selected from the Health Check-up Center and Outpatient Departments of Qilu Hospital of Shandong University(Qingdao).The questionnaire-based survey,physical examinations,biochemical tests,and liver ultrasonography were performed for all cases.Patients were divided into young group(<45 years),middle aged group(45 years≤age<60 years),and old group(≥60 years)according to age,and the clinical features and laboratory findings were analyzed. Results The proportion of male patients gradually decreased with age,while the proportion of female patients increased(P<0.01);The incidences of metabolic diseases showed significant difference among young group,middle aged group,and old group(P<0.01).Except for hyperlipidemia,the proportion of male patients with NAFLD-accompanied metabolic symdrome was significantly higher than that of female patients in all three age groups(all P<0.01). Conclusions The prevalence of NAFLD-accompanied metabolic syndrome disease is associated with age and gender.This finding is useful for the prevention and treatment of NAFLD.

Roles of MicroRNA-21 in the Pathogenesis of Insulin Resistance and Diabetic Mellitus-induced Non-alcoholic Fatty Liver Disease / 中国医学科学院学报

<p><b>OBJECTIVE</b>To investigate the roles of microRNA-21 (miR-21) in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) with high-fat diet-induced insulin resistance (IR) and diabetes mellitus (DM) mice model.</p><p><b>METHODS</b>Eight-week-old C57BL/6 mice were allocated into control group, IR group, and DM group. Body mass was recorded. Intraperitoneal glucose tolerance test was performed to determine any abnormal glucose metabolism. The liver pathological changes were detected by biopsy. Changes in free blood glucose, free serum insulin, blood fat and tumor necrosis factor Α level were measured. Differences in miR-21 expression and peroxidase proliferator-activated receptor subtypes (PPAR-Γ and PPAR-Α) and adipocyte fatty acid binding protein (aP2) in the liver were detected both at the mRNA and protein levels.</p><p><b>RESULTS</b>After one 8-week high-fat diet, the body mass, free serum insulin, and homeostasis model IR index significantly increased in the IR group (P<0.01, P<0.05, compared with control group), while the free blood glucose increased and the free serum insulin decreased in DM group (P<0.05). Free serum insulin level were significantly increased in IR group (P<0.05). Serum tumor necrosis factor-Α levels exhibited an upward trend in control group, IR group, and DM group (P<0.05, P<0.01). With exacerbation in NAFLD, liver miR-21 expression level went further down in both IR and DM groups (P<0.05). The downregulated miR-21 expression level showed negative correlation with upregulated PPAR-Α, ΑP2, and PPAR-Γ genetic expression (r=-0.696, r=-0.664, and r=-0.766, respectively; P<0.05) in IR group and with upregulated PPAR-Α and PPAR-Γ genetic expression in DM group (r=-0.676 and r=-0.550, respectively; P<0.05). In terms of the changes in protein expression level,only on the protein expressions of aP2 and PPAR-Γ in IR group showed significant change (P<0.05, P<0.01, compared with control group).</p><p><b>CONCLUSIONS</b>The miR-21 expression is downregulated in both IR and DM-induced NAFLD mice. It may be involved in the pathogenesis of NAFLD by regulating the expressions of PPAR subtypes.</p>

Effect of COX-2 inhibitor celecoxib on proliferation, apoptosis of HL-60 cells and its mechanism / 中国实验血液学杂志

This study was aimed to investigate the effect of COX-2 inhibitor celecoxib on proliferation, apoptosis of human acute myeloid leukemia cell line HL-60 and its mechanism. HL-60 cells were cultured with different concentrations of celecoxib for 24 h. Cell proliferation was analyzed by CCK-8 assay, cell apoptosis and cell cycle distribution were detected by flow cytometry. Cyclin D1, cyclin E1 and COX-2 mRNA expressions were determined by RT-PCR. The results showed that after the HL-60 cells were treated with different concentrations of celecoxib for 24 h, the cell growth was significantly inhibited in a dose-dependent manner(r = 0.955), IC50 was 63.037 µmol/L of celecoxib. Celecoxib could effectively induce apoptosis in HL-60 cells also in dose-dependent manner(r = 0.988), blocked the HL-60 cells in the G0/G1 phase. The expression of cyclin D1, cyclin E1 and COX-2 mRNA were downregulated. It is concluded that celecoxib can inhibit the proliferation of HL-60 cells in dose-dependent manner, celecoxib causes cell G0/G1 arrest and induces cell apoptosis possibly through down-regulation of the cyclin D1 and cyclin E1 expression, and down-regulation of COX-2 expression respectively.

Coverage on cataract surgery among adults aged 40 or above in a multiethnic rural district of high altitude area in Gongshan county, Yunnan province, China / 中华流行病学杂志

Objective To estimate the prevalence of cataract and its surgical coverage rate together with the burden related to bilateral cataract-blindness,among adults aged 40 or above in Gongshan county of Yunnan province and to evaluate the current cataract status and the efficacy of local cataract prevention program.Methods Cluster sampling was used.The protocol consisted of personal interview,pilot study,visual acuity checking,measuring the intraocular pressure; slit lamp microscopy and the fundus of the eye examination etc.Cataract was graded clinically using the Lens Opacity Classification System (LOCS) ]Ⅲ.Bilateral cataract-blindness burden,bilateral cataractblindness burden and cataract surgical coverage rate were calculated respectively,using two different criteria.Odds ratios (OR) were compared among different groups regarding age,gender,education,ethnic group and altitude of living area.Results Among the 1236 eligible residents,1116 (90.3％)were enrolled in the present study.The prevalence of cataract was 23.8％ among adults aged 40 or order.When the bilateral best refractive vision ＜3/60 was defined as the blindness criterion,the bilateral cataract-blindness burden showed as 1.3％,and cataract blindness surgical coverage rate was 50.0％.When the bilateral presenting vision ＜ 6/60 was defined as the blindness criterion,the bilateral cataract-blindness burden was 25.0％,and cataract blindness surgical coverage rate was 12.9％.The cataract surgical coverage rates were much lower and the bilateral cataract-blindness burden much higher in women,illiterates,living in high altitude areas and those who were aged 70 or above.Conclusion Cataract blindness was a serious public health problem in aged individuals and illiteracy in the residents of the studied areas.Poor prevention programs on cataract called for urgent action to be taken.

Heart-type fatty acid-binding protein alteration in rat's cardiocyte after acute myocardial infarction / 中国应用生理学杂志

<p><b>AIM</b>To explore the changes of mRNA and protein expressions of heart-type fatty acid binding protein (H-FABP) in rat ischemic myocardium at different intervals ischemia.</p><p><b>METHODS</b>60 SD male rats weighing 250-350 g, were randomly divided into one sham-operated group and five study groups (group A1, A2, A3, A4, A5, the left coronary artery of rats has been ligated for 1 h, 2 h, 4 h, 6 h, 12 h respectively). Myocardil samples from infarct zone, ischemic and non-ischemic zone, were obtained for histology examination, and the mRNA for H-FABP in ischemic myocardial tissue were determined by RT-PCR. Serum free fatty acid(FFA) was determined by colorimetric method.</p><p><b>RESULTS</b>Compared to sham hearts, H-FABP mRNA expression were significantly decreased in ischemia zone of AMI rat hearts (P < 0.05), especially in rats underwent 4 h ischemia and 6 h ischemia (P < 0.01). Serum FFA were significantly increased in AMI rats relative to sham rats (P < 0.05).</p><p><b>CONCLUSION</b>Significant down-regulated heart-type fatty acid binding protein after myocardial ischemia might play an important role in myocardial injury and energy metabolism disorder.</p>

Hemin, a heme oxygenase-1 inducer, improves aortic endothelial dysfunction in insulin resistant rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Under an insulin resistance (IR) state, overproduction of reactive oxygen species (ROS) may be playing a major role in the pathogenesis of endothelial dysfunction, hypertension and atherosclerosis. Recently, increasing attention has been drawn to the beneficial effects of heme oxygenase-1 (HO-1) in the cardiovascular system. This study aimed to investigate the effects of HO-1 on vascular function of thoracic aorta in IR rats and demonstrate the probable mechanisms of HO-1 against endothelial dysfunction in IR states.</p><p><b>METHODS</b>Sprague-Dawley (SD) rats fed with high-fat diet for 6 weeks and the IR models were validated with hyperinsulinemic-euglycemic clamp test. Then the IR rat models (n = 44) were further randomized into 3 subgroups, namely, the IR control group (n = 26, in which 12 were sacrificed immediately and evaluated for all study measures), a hemin treated IR group (n = 10) and a zinc protoporphyrin-IX (ZnPP-IX) treated IR group (n = 8) that were fed with a high-fat diet. Rats with standardized chow diet were used as the normal control group (n = 12). The rats in IR control group, hemin treated IR group and ZnPP-IX treated IR group were subsequently treated every other day with an intraperitoneal injection of normal saline, hemin (inducer of HO-1, 30 micromol/kg) or ZnPP-IX (inhibitor of HO-1, 10 micromol/kg) for 4 weeks. Rats in the normal control group remained on a standardized chow diet and were treated with intraperitoneal injections of normal saline every other day for 4 weeks. Systolic arterial blood pressure (SABP) was measured by tail-cuffed microphotoelectric plethysmography. The blood carbon monoxide (CO) was measured by blood gas analysis. The levels of nitric oxide (NO), inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), blood glucose (BG), insulin, total cholesterol (TC) and triglyceride (TG) in serum, and the levels of total antioxidant capacity (TAOC), malondialdehyde (MDA) and superoxide dismutase (SOD) in the aorta were measured. The expression of HO-1 mRNA and HO-1 protein in aortal tissue were detected by semi-quantitative RT-PCR and Western blot. The vasoreactive tensometry was performed with thoracic aortic rings (TARs).</p><p><b>RESULTS</b>Compared with the normal control group, the levels of SABP, BG, insulin, TC, TG, NO, iNOS and MDA were higher, while the levels of CO, TAOC, SOD and eNOS were lower in IR control rats. After treatment of IR rats for 4 weeks a more intensive expression of HO-1 mRNA and HO-1 protein were observed in hemin treated IR group compared with the normal control group. And compared with 4-week IR control rats, the levels of CO, TAOC, SOD and eNOS were increased, while the levels of SABP and iNOS activity were lower in the hemin treated IR group. Administration of hemin in IR rats appeared to improve the disordered vasorelaxation of TARs to acetylcholine (ACh). Alternatively, the reverse results of SABP, CO, TAOC, SOD, iNOS and vasorelaxation responses to ACh were observed in IR rats with administration of ZnPP-IX.</p><p><b>CONCLUSIONS</b>The endothelial dysfunction in the aorta is present in the IR state. The protective effects of HO-1 against aortic endothelial dysfunction may be due to its antioxidation and regulative effect of vasoactive substances. It is proposed that hemin, inducer of HO-1, could be a potential therapeutic option for vascular dysfunction in IR states.</p>

The role of activation of nuclear factor-kappa B on the expression of heme oxygenase-1 induced by lipopolysaccharide in rat myocardium / 中国应用生理学杂志

<p><b>AIM</b>The role of activated nuclear factor-kappa B(NF-kappaB) on the expression of heme oxygenase-1 induced by lipopolysaccharide (LPS) in rats' myocardium was obversed, and the effect exerted in endotoxic shock was explored.</p><p><b>METHODS</b>The changes in mean arterial pressure within 12 hours were recorded on a polygraph. The protein expression of NF-kappaB p65 in rats'myocardium, which were induced by lipopolysaccharide were measured with immunochemistry. The changes both of protein and gene expression of heme oxygenase-1 in rats' myocardium, which were induced by injection of LPS or preadministration of the specific inhibitor of NF-kappaB, pyrrolidine dithiocarbamate(PDTC), were examined by immunochemistry of reverse transcripted polymerase chain reaction.</p><p><b>RESULTS</b>(1) LPS caused a rapid decrease of MAP within 12 h( P < 0.01). (2) After LPS was administration, the protein expression of NF-kappaB p65 in both of micrangium endothelium within myocardium markedly increased at 0.5 h and 2 h, while decreased gradually at 6 h and 12 h. (3) ES group expressed as migration of acute inflammatory cells and dilation and stagnation in blood capillary, while the increase of HO-1 mRNA induced by LPS didn't change at the first 0.5 h, began at 2 h, peaked at 6 h, and declined at 12 h, respectively. The protein expression of HO-1 in micrangium endothelium within myocardium markedly increased and emerged in myocardium, and kept a high level at 6 h and 12 h. (4) When a specific inhibitor of NF-kappaB, PDTC, was applied to inhibit the level of NF-kappaB, we found that the pathomorphological changes of myocardium in ES rats were improved and both HO-1 mRNA and protein expression in myocardium markedly failed at 6 h.</p><p><b>CONCLUSION</b>NF-kappaB was activated on the stimulation of LPS, which brought about its translocation to the nucleus to act on transcription activity of HO-1 gene. NF-kappaB might be involved in its signal transductive mechanisms, which might be one of the important mechanism of LPS inducing the refractory low arterial pressure in ES rats.</p>

The dynamic changes of heme oxygenase-1 mRNA and protein express at subfornical organ in rats with experimental allergic encephalomyelitis / 中国应用生理学杂志

<p><b>AIM</b>To observe the dynamic changes of heme oxygenase-1 (HO-1) mRNA and protein express in subfornical organ in rats with experimental allergic encephalomyelitis (EAE) to confirm that SFO is one of the sites for blood-bearing signaling molecules entering into brain.</p><p><b>METHODS</b>EAE was induced by CFA-GPSCH on Wistar rats, we observed the levels of HO-1 mRNA and its protein expression with immunohistochemistry and in situ hybridization technology on 1 d, 7 d, 14 d, and 21 d after EAE induction in SFO of rats. The relationship between HO-1 and symptoms of EAE was also investigated.</p><p><b>RESULTS</b>The expression levels of HO-1 mRNA and its protein expression were very low in the brains of the control group, whereas they were enhanced gradually with pathological course in the brain and onsets of symptoms, signs of EAE. On 1 d after induction of EAE, positive cells of HO-1 mRNA and its protein expression were observed at SFO, but the labeled cells were rarely seen in the other brain regions. On 7 d, the positive cells increased markedly. On 14 d the levels of HO-1 mRNA and its protein expression in the brains reached the peak, the positive cells of HO-1 were mainly located at the choroid plexuses and SFO, as well as the regions around "sleeve-like" lesion foci, all of which were coincident with the locations of lesions of EAE. The changes of incidence, symptom, reduction of the body weight, and pathology lesions of EAE in rat brains were the most significant. On 21 d, the levels of HO-1 mRNA and its protein expression reduced gradually, which was in parallel with remitted symptoms of EAE. When a specific inhibitor of HO-1, Snpp9, was applied, the symptoms and pathological lesions of EAE in brains were mitigated markedly.</p><p><b>CONCLUSION</b>SFO may be one of the earliest sites for blood-bearing signaling molecules entering into brain. The dynamic changes of HO-1 mRNA and its protein expression are in parallel with the changes of symptoms and pathological lesions of EAE in the brains. Application of some inhibitors of HO-1 may be one of potential therapeutic methods for prevention and treatment of EAE.</p>

Melatonin improves vascular reactivity of endotoxemia rats / 生理学报

The purpose of the present study was to investigate the effect of melatonin (MT) on the abnormal reactivity of thoracic aorta and pulmonary artery induced by lipopolysaccharide (LPS) in rats. Sprague-Dawley rats were divided into four groups randomly: (1) Vehicle group; (2) LPS group: LPS (4 mg/kg, i.p.); (3) LPS+MT group: MT (5 mg/ml, i.p.) was given 30 min before LPS and 60 min after LPS (4 mg/kg ,i.p); (4) MT group: received two doses of MT, 90 min after the first injection of MT another dose of MT was given. Six hours after LPS injection,the rats were killed and both thoracic aortic rings (TARs) and pulmonary artery rings (PARs)were prepared. The reactivity of TARs and PARs in the four subgroups was tested separately. The contraction response to phenylephrine (PE) and the endothelium-dependent relaxation response (EDRR) to ACh were observed with the isolated artery ring technique. Concentration-response curves were generated with ACh or PE (1 x 10(-8) - 1 x 10(-5) mol/L). Superoxide dismutes (SOD) activity and the content of malondialhyde (MDA) in artery tissues were detected. For TARs, LPS significantly reduced the contraction response to PE compared with the vehicle group (P<0.01) and the curve of cumulative dose responses to PE in the LPS group shifted downward. Although EDRR to ACh in the LPS group had the tendency to decrease but still showed no significant difference compared with the vehicle group (P>0.05). For PARs, EDRR to ACh was depressed significantly in the LPS group (P<0.01), while no effect on contraction response to PE in the LPS group was observed, compared with the vehicle group (P> 0.05). Compared with the LPS group, TARs in the LPS+MT group exhibited an increased contraction response to PE, but were still lower than that in the vehicle group. Similarly, EDRR to ACh of PARs in the LPS+MT group was improved significantly and there was no difference between the LPS+MT group and the vehicle group. The vascular reactivity was unaffected in MT group compared with the vehicle group in both TARs and PARs. SOD activity in the LPS +MT group increased significantly and the content of MDA decreased markedly compared with the LPS group. These results suggest that MT may improve the vascular reactivity in endotoxemia rats due to its antioxidant properties.

Cholecystokinin octapeptide increases free intracellular calcium of guinea pig cardiomyocytes through activation of Ca2+ channel and tyrosine kinase / 生理学报

The aim of the present study was to explore the effect of cholecystokinin octapeptide (CCK-8) on [Ca(2+)](i) and its signal transduction mechanism in isolated guinea pig cardiomyocytes. [Ca(2+)](i) was measured by laser scanning confocal microscopy in single ventricular myocytes which were dissociated by enzymatic dissociation method and loaded with Fluo 3-AM. The changes in [Ca(2+)](i) were represented by fluorescent intensity (F(i)) or relative fluorescent intensity (F(i)/F(O)%). The results obtained are as follows. (1) In the normal Tyrode's solution containing 1.0 mmol/ L Ca(2+), CCK-8 (1-10(4) pmol/L) elicited a rapid and marked increase in [Ca(2+)](i). (2) When cardiomyocytes were pretreated with the Ca(2+) chelator EGTA (3 mmol/L) and Ca(2+) channel antagonist nisoldipine (0.5 micromol/L) for 5 min, CCK-8 (10(2)pmol/L) caused a slow and small increase in [Ca(2+)](i) (p< 0.01). (3) Pretreatment with the nonselected CCK- receptor (CCK-R) antagonist proglumide (6 micromol/L) or the tyrosine kinase inhibitor genistein (1 micromol/L) for 5 min could inhibit the increase of [Ca(2+)](i) induced by CCK-8 (10(2) pmol/L) (p<0.01). The results suggest that CCK-8 increases the [Ca(2+)](i) via activating the receptor-operated Ca(2+) channel and eliciting the influx of Ca(2+) in isolated guinea pig cardiomyocytes, in which tyrosine kinase may be involved.

Dynamic changes of heme oxygenase-1 protein and mRNA in the brains of rats with experimental allergic encephalomyelitis / 生理学报

In order to investigate the role of heme oxygenase-1 (HO-1) in the molecular mechanism of experimental allergic encephalomyelitis (EAE), which was induced by guinea pig spinal cord homogenate + complete freund adjuvant on Wistar rats, we observed the gene of HO-1 and its protein expression with reverse transcriptase polymerase chain reaction(RT-PCR) and immunohistochemistry 1, 7, 14, and 21 d after EAE induction in rats. The relationship between HO-1 and the symptoms of EAE was also observed. The results showed that the levels of HO-1 mRNA and its protein expression were very low in the brains of the control group, whereas they were enhanced gradually with pathological course in the brain and onsets of symptoms, signs of EAE. On day 7, the level of HO-1 mRNA reached the peak, but the expression level of HO-1 protein in the brains reached the peak on day 14. The immunoreactive cells of HO-1 were mainly located at the choroid plexuses and subfornical organ (SFO), as well as in regions around the "sleeve-like" lesion foci, all of which were coincident with the locations of lesions of EAE. The levels of HO-1 mRNA and its protein expression were lowered gradually on day 21, which were in parallel with the severities of symptoms and signs of EAE. After a specific inhibitor of HO-1, Snpp-9, was applied, both of the symptoms and pathological lesions of EAE in the rat brains were mitigated markedly. Therefore, these results may suggest that the dynamic changes of HO-1 mRNA and its protein expression are in parallel with the changes of symptoms and pathological lesions of EAE in the brain. In conclusion, the levels of HO-1 mRNA and its protein expression in brains may play an important role in the pathogenesis of EAE, and application of inhibitors of HO-1 may be one of the potential therapeutic ways for the prevention and treatment of EAE.

The role of activation of nuclear factor-kappa B of rat brain in the pathogenesis of experimental allergic encephalomyelitis / 生理学报

To investigate the role of activated nuclear factor-kappaB (NF-kappaB) in experimental allergic encephalomyelitis (EAE), the activity and protein expression of NF-kappaB p65 in rat brain tissues, which were extracted from EAE rats at 1, 7, 14 and 21 d respectively after EAE was induced by CFA-GPSCH, were measured with electrophoretic mobility shift assay and immunohistochemistry. The relationship between activated NF-kappaB and symptoms of EAE was also investigated. The results showed that protein expression level and the activity of NF-kappaB were very low in the brain of the control group. After EAE was induced, the activity of NF-kappaB and the level of the protein expression in the brains increased gradually with the development of symptoms and brain pathology of EAE. On d 14, both the activity and the level of protein expression in the brains reached a peak, the positive cells of NF-kappaB were mainly located at the choroid plexuses and subfornical organ, as well as around the regions of sleeve-like lesion foci, which were coincident with the locations of lesions of EAE. The incidence, symptoms, reduction of the body weight and pathology of EAE rats brains at the above locations were most significant. On d 21 the activity of NF-kappaB and level of the protein expression reduced gradually, which was in parallel with a gradual alleviation of the symptoms of EAE rats. After a specific inhibitor of NF-kappaB, PDTC was applied, the symptoms and pathological lesions of EAE rat brain were mitigated markedly. The above results indicate that the dynamic changes in the activity and protein expression of NF-kappaB were in parallel with the changes in symptoms and pathological lesion of EAE rat brains. In conclusion, the activated NF-kappaB in the brain may play a critical role in the pathogenesis of EAE, and application of some inhibitors of NF-kappaB, such as PDTC, may be one of the effective therapeutic methods for prevention and treatment of EAE.

Expression of heme oxygenase-1 induced by lipopolysaccharide in thoracic aortic and its effect on vascular reactivity / 中国应用生理学杂志

<p><b>AIM</b>To explore the effects of heme- heme oxygenase-1 (HO-1)-carbon monoxide(CO)-cyclic GMP (cGMP)on aortic vascular reactivity in endotoxemic rats and its molecular mechanism.</p><p><b>METHODS</b>By using isolated vascular ring tension detecting technique, cumulative responses of thoracic aortic rings (TARs)to phenylephrine (PE) were measured at 6 h after lipopolysaccharide administration. Effects on contractile responses to PE were measured under which the TARs were incubated with hemin (He, donor of CO), zinc-protoporphyrin-IX(ZnPP-IX, selective inhibitor of HO-1), or methylene blue (MB, inhibitor of guanylyl cyclase), respectively. The content of CO and the activity of HO-1 were measured. The protein and the gene expression of HO-1 were examined by Western blot and RT-PCR.</p><p><b>RESULTS</b>Contractile responses of TARs to cumulative doses of PE were depressed by pretreated with LPS. The hyporesponsiveness was partly reversed by incubation with ZnPP-IX and was restored to normal by incubation with MB in endotoxemic rats. Incubation with He could contribute to the vascular hyporeactivity. The content of CO, the activity and the protein and the gene expression of HO-1 were significantly increased in aorta of endotoxemic rats.</p><p><b>CONCLUSION</b>LPS could induce the HO-1 mRNA and the protein expression, the activity of HO-1 increase in aorta, lead to active the pathway of heme-HO-1-CO-cGMP, which is one of the important mechanisms of the vascular hyporeactivity in endotoxemic rats.</p>

Inhibitory effect of cholecystokinin-octapeptide on production of cytokines in the lung of endotoxic shock rats / 生理学报

To study the effect of cholecystokinin-octapeptide (CCK-8) on systemic hypotension and cytokine production in serum and lung of endotoxic shock (ES) rats induced by lipopolysaccharide (LPS) and investigate its signal transduction mechanism of p38 mitogen-activated protein kinase (MAPK), the changes in mean arterial pressure (MAP) were observed by using a polygraph in four groups of SD rats: group of LPS (8 mg/kg i.v.) induced ES, group of CCK-8 (40 microg/kg i.v.) pretreatment 10 min before LPS (8 mg/kg) administration, group of CCK-8 (40 microg/kg i.v.) only, and normal saline (control) group; the contents of proinflammatory cytokines (TNF-alpha, IL-1 beta and IL-6) in the lung and serum were assayed using ELISA kits; and p38 MAPK was detected by Western blot. The results showed that CCK-8 alleviated LPS-induced decrease in MAP of rats; compared with the control, LPS elevated the levels of TNF-alpha, IL-1 beta and IL-6 in serum and lung significantly, while CCK-8 significantly inhibited the LPS-induced increases in TNF-alpha, IL-1 beta and IL-6 in serum and lung. The activation of p38 MAPK in the lung of ES rats was enhanced by CCK-8 pretreatment. These results suggest that CCK-8 can alleviate the LPS-induced decrease in MAP of ES rats and exert an inhibitory effect on the overproduction of proinflammatory cytokines, and that p38 MAPK may be involved in its signal transduction mechanisms.

Effects of cholecystokinin octapeptide on rat cardiac function and the receptor mechanism / 生理学报

The aim of this study was to explore the effects of cholecystokinin octapeptide (CCK-8) on cardiac function and the receptor mechanism in anesthetized rats. The mean arterial pressure (MAP), heart rate (HR), the left ventricle systolic pressure (LVP) and the maximal/minimum rate of LVP (+/-LV dp/dt(max)) were measured. The results obtained are as follows. (1) Low dose of CCK-8 (0. 4 microgram/kg i.v.) caused tachycardia and slight increase in MAP, LVP and LV dp/dt(max) (P<0.01), while medium dose (4.0 microgram/kg i.v.) and high dose of CCK-8 (40 microgram/kg i.v.) elicited a bradycardia and marked increase in MAP, LVP and LV dp/dtmax (P<0.01). (2) Proglumide (1.0 mg/kg i.v.), a CCK-receptor (CCK-R) antagonist, significantly inhibited the pressor effects of CCK-8, whilst it reversed the bradycardic responses (P<0.01). (3) Using reverse transcription polymerase chain reaction (RT-PCR), CCK-A receptor (CCK-AR) and CCK-B receptor (CCK-BR) mRNA were expressed in myocardium of rats. The above results indicate that CCK-8 may enhance cardiac function in a dose-dependent manner and elicit a change in HR, which is likely induced by the activation of CCK-R on myocardium.