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Objective·To observe mitochondria permeability transition pore (mPTP) opening and apoptosis of H9c2 myocardial cell stimulated by lipopolysaccharide (LPS),and to explore the anti-apoptotic effect of combined application of cyclosporine A (CsA) and ryanodine (Rya).Methods·The H9c2 cells were divided into Control group,LPS group,LPS+CsA group,LPS+Rya group,and LPS+CsA+Rya group.The mPTP opening state,Ca2+ concentration within cell and mitochondrial,mitochondrial membrane potential (AΦm),cell apoptosis,expression of Bax and Bcl-2 at mRNA and protein levels,and activity of caspase 3 were determined respectively.Results·mPTP opened after being stimulated by LPS for 24 h,which increased the fluorescence intensity for Ca2+in cytosolic and mitochondria by 298％ and 231％ respectively,induced about 1/3 cell apoptosis,improved the activity of caspase 3 approximately twice,and enhanced expression ofBax mRNA (P=0.008).The combined use of CsA and Rya effectively inhibited mPTP opening,increased the enhancement of fluorescence intensity for Ca2+in both cytosolic and mitochondria,maintained normal AΦrn,reduced LPS-induced apoptosis,inhibited the activity of caspase 3,and decreased Bax mRNA expression level induced by LPS in the myocardial cells.Conclusion·mPTP plays an important role in in LPS-induced myocardial apoptosis,whereas the combination of CsA and Rya can alleviate it effectively.
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Objective To investigate the changes of serum adiponectin level and insulin resistance in patients with obstructive sleep apnea hypopnea syndrome (OSAHS).Methods 80 adult habitual snorers were divided into mild,moderate,severe OSAHS groups and control group,based on their apnea hypopnea index (AHI).Correlative clinical data were measured and analyzed.Results Serum adiponectin level [( 5.44 ± 2.57 ) mg/L] was significantly lower and HOMA-insulin resistance index ( 3.42 ± 0.70) was significantly higher in severe group than other groups ( P ＜ 0.05 ).Serum adiponectin level was negatively correlated with BMI,waist hip ratio,neck circumferences and et al( r =-0.233 ～ -0.499,P ＜0.05),but it was positively correlated with lowest oxygen saturation ( LSaO2 ),Ⅲ + Ⅳ％ and REM％ ( r =0.270～ 0.429,P ＜ 0.05).Conclusions Both hypoadiponectinemia and insulin resistance were observed in severe OSAHS patients.The related risk factors of hypoadiponectinemia in OSAHS might include obesity,disordered sleep architecture and other adipokines.
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Objective To investigate the role of calcitonin gene-related peptide(CGRP)and IP3 signal pathway in ischemic preconditioning(IPC)in the isolated perfused hearts of rats with type 1 diabetes mellitus. Methods Type 1 diabetes mellitus rat models were established in 80 SD rats,and were randomly divided into 4 week(D-4w)group and 8 week (D-8w)group.These two groups were randomly subdivided into model control(D-Cont)group,type 1 diabetes mellitus ischemia-reperfusion(IR)group,IPC group,CGRP(IPC+CGRP)group and IP3 inhibitor wortmanin(IPC+WMN) group.Another 16 rats were served as normal control(N-Cont)group.In vitro perfusion models of isolated hearts were established by Langendorff methods,and CGRP or wortmanin(WMN)were administered during perfusion.The left ventricle function of isolated heart in each group was monitored by multichannel biosignal analysis system,and coronary artery flow was recorded.The serum CGRP levels were detected by ELISA.The activity of lactate dehydrogenase(LDH)and creatine kinase(CK)in effluent of coronary artery was detected by biochemical method.The size of myocardial infarction was determined by NBT staining,and apoptosis of cadiocytes was detected by TUNEL method. Results Compared with N- Cont group,the CGRP level in serum of rats with type 1 diabetes mellitus decreased with time,the basic left ventricle function decreased,while the activity of LDH and CK in effluent of coronary artery,size of myocardial infarction and cardiomyocyte apoptosis index increased(P<0.05).Compared with N-Cont group,the left ventricle function was significantly lower in IR group,and more severe myocardial damage was observed.IPC improved myocardial damage of D-4w IR group,while had no protection on D-8w IR group.Compared with IPC group,the left ventricle function was significantly improved in IPC+CGRP group.IPC+WMN blocked the myocardial protection of D-4w group from IPC.Conclusion CGRP and IP3 signal pathway are involved in the protection provided by IPC in isolated hearts of rats with type 1 diabetes mellitus.
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Objective To explore the correlation between Chlamydia pneumoniae (Cpn) infection and sudden sensorineural hearing loss (SSHL). Methods One hundred and twenty patients with SSHL were enrolled as SSHL group, and another 120 healthy subjects were served as control group. Human peripheral blood mononuclear cells (PBMCs) were isolated, and the expression of Cpn-specific antigen (Cpn-Ag) and Cpn-DNA in PBMCs was detected by direct immunofluorescence test and PCR, respectively. Specific antibodies (IgA, IgG and IgM) to Cpn were determined by microimmunofluorescence test.Results There was no significant difference in the positive findings between direct immunofluorescence test and PCR (P>0.05). There were significant differences in the positive rates of Cpn-Ag and Cpn-IgM for acute infection between these two groups (P＜0.01), and there were significant differences in the positive rates of Cpn-IgA and Cpn-IgG for chronic infection between these two groups (P＜0.05). Conclusion There is a significantly higher prevalence of Cpn in patients with SSHL. Cpn infection may be a possible cause for SSHL.
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Objective To investigate the protective effects of recombinant human tumor necrosis factor receptor:Fc fusion protein (rhuTNFR:Ice)on the acute renal injury induced by lipepelysaccharide(LPS)in rats.Methods Models ofacute renal injury in rats were constructed by intravenous injection of LPS 10 m/kg.Forty-eight SD rats weighing 180～240g were randomly divided into 4 groups with 12 animals each group,including control group,rhuTNFR:Fc group,LPS groupand rhuTNFR:Fc+LPS group.Mean arterial pressure(MAP)wKs continuously monitored for 6 h.The levels of blood tLrea nitrogen(BUN)。Creatinine(Cr),TNF-αas well as TNF-α bioactivity were assessed.The myeloperoxinse(MPO)and superoxide dismutase(SOD)activity,content ofmalondialdehyde(MDA)were also measured.Pathologic changes of lung tissue in each group were observed by HE staining.Results Compared with LPS group,the status of hypotension and pathological manifestation in kidneys were ameliorated,and MPO activity significantly decreased in rhuTNFR:Fc+LPS group(P<0.05).Conclusion These data suggest that rhuTNFR:Fc can ablate the rise in serum TNF-α bioactivity that occurs in response to LPS,and rhuTNFR:Fc could in part protect rats from the acute renal injury induced by LPS.
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Objective To investigate the protective effects and the undedying mechanism of recombinant human tumor necrosis factor receptor: Fc fusion protein (Yisaipu, rhu TNFR: Fc) on the lipopolysaccharide (LPS) induced acute liver injury of rats. Method Totally48 SD rats were randondy divided into four groups , in-cluding control gronp (n = 12), Yisaipu group(n = 12), LPS gronp(n = 12) and Yisaipu + IPS group(n = 12). The models of acute liver injury were produced by injection of LPS intravenously. Being fasted for 12 h, the rats were anaesthetized (60 mg/kg pentobarbital sodium, i.p.) and cannulated into carotid arteries. The cannula was connected with the multi-channel creature signal analysis system. The rata in control group and LPS group were injected with normal saline or LPS in dose of 5 mg/kg through rats' sublingual vein respectively. While the rats in Yisaipu group and Yisaipu + LPS group was pretreated with Yisaipu in dose of 0.4 mg/kg subcutaneously 24 h be-fore normal saline or LPS infusion. Six rats of each goup were randomly selected and mean arterial pressure (MAP) were monitored for 6 h via multi-channel creature signal analysis system, and rats' survival rate was calcu-lated. The rats whose MAP less than 10 mmHg were considered to die and the alive rats during period of observa-tion sacrificed by exsanguination. The liver tissue at the same site was removed, fixing in 10% formalin or stored at -80 ℃. To detect serum TNF-α, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) level, 0.2 mL blood samples were collected from the carotid artery 2 and 3 h after the injection of saline or LPS. The serum was collected from centrifuged blood samples and stored at -80 ℃. Enzyme-linked immunosorbent assay (ELISA) and flow cytometry were used to assess serum TNF-α level and bioactivity respectively. We also measured the serum ALT and AST levels, the myeloperoxiase (MPO) and superexide dismutase (SOD) activity, and malon-dialdehyde (MDA) content in liver tissue The pathology of hepatic tissue was evaluated by HE staining. Statistical-ly,the data of TNF-α level and bioactivity, ALT and AST release, and MDA content were analyzed by ANOVA, and rat survival rate were analyzed by Chi-square Tests. Results The rats in control group and Yisaipu group were all survived. Rat survival rate was significantly higher in Yisaipu + LPS group (67%) than in LPS group (17%) (P < 0.05). Serum TNF-α bioactivity was significantly lower in Yisaipu + LPS group than in LPS group [(7.3±2.8)% vs.(51.3±6.4)%, P <0.05]. Compared with IPS group, Yisaipu pretreatment decreased MDA content [(1.40±0.10)vs. (2.81±0.11) nmol/mgprot, P <0.05]and MPO acticity [(0.38±0.04) vs. (0.54±0.02) U/g, P <0.05]in hepatic tissue, while SOD activity [(188.4±20.2) vs. (142.5 ± 18.3) U/mgprot, P <0.05]was increased. The serum AST level, ALT level and the pathology in the liver were also ameliorated correspondingly. Conclusions These data suggest that Yisaipu could protect rats from LPsinduced a-cute liver injury by inhibiting TNF-α bioactivity and by enhancing anti-oxidation.
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Renovascular hypertensive rats were treated with either medipine (m-Nif) or nifedipine (Nif) for 9 weeks. In all groups the antihypertive therapies significantly reduced both mean arterial blood pressure and left ventricular hypertrophy. In LVH rats contractions caused by NE were increased on rings both with endothelium and without endothelium, and NE-ratio was greater than 1. The increase in NE induced contraction and the decrease in Ach induced relaxation in LVH rats were due to bothendothelium and smooth muscle dysfuction. In the m-Nif and Nif treated groups, these NE-ra-tio were significantly decreased and had lower maxtimal response and higher IC50. These indicate m-Nif and Nif had direct effect on smooth muscle and endothelium. Our results show that m-Nif and Nif has no influence on the endotheli-um-dependent relaxation to Ach.