Objective To investigate inhibitory effect of Telmisartan on carotid arterial intima-media thickness in patients with essential hypertension. Methods 104 patients with mild or mid essential hypertension were randomly divided into three groups, which include telmisartan group( telmisartan 80 mg/d PO), ramipril group( ramipril 5 mg/d PO), and control group( other anti-hypertension agents). Blood pressure was monitored during treatment. Carotid arterial intima-media thickness(CIMT) were measured in all patients at beginning and patients who had the 12 months course. Results There were 91 patients who had the 12 months course,which include telmisartan group33 cases,ramipril group28 cases, and control 30 cases. The CIMT was significantly decreased in telmisartan group and ramipril group ( all P < 0. 05 ), and not changed in control while blood pressure fall effectively. In ramipril, group5 cases were ceased the course because of severe cough. Conclusion Both telmisartan and ramipril could decrease blood pressure and CIMT effectively, and there were less side effects in telmisartan group.

Aim To investigate the role of ATP-sensi-tive potassium channels-Akt pathway in exogenous hy-drogen sulfide( H2 S) inhibiting the high glucose( HG)-induced injury in H9c2 cardiac cells. Methods The expression level of Akt protein was tested by Western blot assay. The cell viability was measured by cell counter kit-8(CCK-8 assay). The number of apoptotic cells was tested by Hoechst 33258 nuclear staining fol-lowed by photofluorography. The intracellular levels of reactive oxygen species ( ROS ) were detected by DCFH-DA staining followed by photofluorography. Mi-tochondrial membrane potential ( MMP ) was examined by JC-1 staining followed by photofluorography. Results H9c2 cells were treated with 35 mmol·L-1 glucose (high glucose, HG) for 0 ~24 h respectively. After treating for 3 h, the expression level of phosphorated ( p )-Akt protein began to be obviously reduced, the maximum reduced expression level was observed after the cells were exposed to HG for 24 h. Pretreatment of the cells with 50 μmol · L-1 pinacidil ( Pin, a KATP channel opener) or 400 μmol·L-1 NaHS( a donor of H2 S) prior to exposure to HG considerably blocked the down regulation of p-Akt expression level induced by HG. However, pretreatment with 1 mmol · L-1 KATP channel blocker glibenclamide( Gli) obviously attenua-ted the inhibitory effect of NaHS on HG-induced down-regulation of p-Akt expression level. On the other hand, the protective effects of NaHS against the HG-induced cardiomyocyte injury were markedly blocked by 30 μmol·L-1 Ly294002(an inhibitor of Akt), as indicated by the decrease in cell viability and MMP dissipation as well as the increases in the number of apoptotic cells and ROS generation. Conclution KATP channels-Akt pathway mediates the protective effect of H2 S against the HG-induced cardiac injury.

Aim To investigate whether nicorandil (Nic)protects H9c2 cardiac cells against high glucose (HG)-induced injury and inflammation by inhibiting nuclear factor-κB (NF-κB )/cyclooxygenase-2 (COX-2 )pathway.Methods Cell viability was measured by cell counter kit-8 (CCK-8)assay.The expression lev-els of NF-κB,COX-2 and cleaved caspase-3 were de-termined by Western blot.The activity of lactate dehy-drogenase (LDH)in the culture medium was measured with commercial kits.The intracellular level of reactive oxygen species (ROS)was detected by 2′,7′-dichlor-fluorescein-diacetate (DCFH-DA)staining followed by photofluorography.The number of apoptotic cells was observed by Hoechst 33258 nuclear staining followed by photofluorography.Mitochondrial membrane poten-tial (MMP)was examined by rhodamine 123 staining followed by photofluorography.The secretion levels of interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) were detected by ELISA.Results After H9 c2 cardiac cells were treated with 35 mmol · L-1 glucose (high glucose,HG)for 24 h,the cell viability was significantly decreased .Pre-treatment of the cells with 20~100 μmol·L-1 Nic for 60 min or 50 μmol· L-1 Nic for 30~120 min before exposure to HG signif-icantly attenuated the decrease in viability induced by HG.On the other hand,HG increased the expression levels of phosphorated (p)-NF-κB p65 and cyclooxy-genase-2 (COX-2 )in H9c2 cardiac cells.Pre-treat-ment of the cells with 50 μmol·L-1 Nic for 60 min at-tenuated the up-regulation of p-NF-κB p65 and COX-2 expression levels induced by HG.Furthermore,HG induced considerable injuries and inflammatory re-sponse,leading to increases in LDH activity,ROS generation,MMP loss,the number of apoptotic cells, the expression of cleaved caspase-3 as well as the se-cretion levels of IL-1βand TNF-α.Pre-treatment of the cells with 50 μmol·L-1 Nic for 60 min before HG exposure,or co-treatment of the cells with 100 μmol· L-1 PDTC (an inhibitor of NF-κB)or 10 μmol·L-1 NS-398 (an inhibitor of COX-2)and HG for 24 h ob-viously reduced the above injuries and inflammatory re-sponse induced by HG. Conclusion Nic protects H9 c2 cardiac cells against HG-induced injury and in-flammation by inhibiting NF-κB/COX-2 pathway.

OBJECTIVE: To evaluate the efficacy and safety of Pravastatin versus Simvastatin in downregulating low density lipoprotein cholesterol(LDL-C) and upregulating high density lipoprotein cholesterol(HDL-C).METHODS: A total of 66 patients with hypercholesterolemia were enrolled: 33 were randomly assigned to receive Pravastatin(40 mg) for 6 weeks,and another 33 to receive Simvastatin(40 mg) for 6 weeks.Serum lipid levels at baseline and 6 weeks after medication were measured.The primary effective indicator was LDL-C as compared with baseline value and the secondary effective indicator was HDL-C.Safety was evaluated based on laboratory data and clinical adverse reactions.RESULTS: Both Pravastatin and Simvastatin significantly decreased LDL-C level,showing significant differences as compared with before medication(P0.05).Less adverse drug reactions were noted in both groups.CONCLUSION: Pravastatin and Simvastatin were equivalent in lipid-regulatory effect and both were well-tolerated.

[Objective] To investigate the inhibitory effect of CTLA-4Ig fusion protein on atherosclerosis in the mice with an apolipoprotein-E gene defect fed on cholesterol diet.[Methods] Twenty-five male 10-week-old ApoE-/- mice were selected and fed on cholesterol diet for 4 weeks,5 out of which were executed at random as control group and their pathological sections were kept to observe the early fatty streaks.The other 20,divided into CTLA-4Ig treatment group,PBS group,IgG1 group,and blank group at random,5 in each.Three groups were given intraperitoneal injection of CTLA-4Ig (10 μg per time),PBS (100 μL per time),Rat-IgG1 (10 μg per time) respectively,twice a week,for 8 weeks.The blank group has no treatment.Followed by 8-week treatment,the whole aorta from the root to crotch of iliac artery was separated after anesthesia with the intraperitoneal injection of 1 % pentobarbital.Subsequently,the area ratio of plaque and lumen,the thickness ratio of endangium and tunica media,the lipid-soaking extent intra-plaque and the content of collagen fibrils and smooth muscle cells intra-plaque were analyzed by image-processing soft.[Results] After fed on cholesterol diet for 4 weeks,there were obviously atherosclerosis in the aorta in the ApoE-/- mice.There were typical atherosclerotic plaque in ApoE-/- mice fed on cholesterol diet after another 8 weeks.The area ratios of plaque and lumen in CTLA-4Ig group,PBS group,IgG1 group,and blank group were 0.27 ± 0.08,0.40 ± 0.08,0.43 ± 0.08,and 0.46 ± 0.10,and obviously increased than those in control group (0.05 ± 0.01,P ＜ 0.05).The thickness ratios of endangium and tunica media in four groups were 2.6 ± 0.6,6.0 ± 0.9,5.7 ± 0.8,and 5.9 ± 0.6 and obviously increased than those in control group (0.5 ± 0.1,P ＜ 0.05).The lipid-soaking extent intra-plaque in experimental groups were 26.0 ± 3.0,40.8 ± 5.7,40.6 ± 3.0,and 43.2 ± 5.7,and were obviously increased than those in control group (7.2 ± 1.4,P ＜ 0.05 ).It was found that the area ratio of plaque and lumen,the thickness ratio of endangium and tunica media,and the lipid-soaking extent intra-plaque in CTLA-4Ig group were significantly lower than those in PBS group,IgG1 group,and blank group (P ＜ 0.05),but there was no significant difference in those between the PBS group,IgG1 group,and blank group (P ＞ 0.05).The content of collagen fibrils in CTLA-4Ig group were 16.0 ± 1.1 and higher than those in PBS group,IgG1 group,and blank group (8.6 ± 1.2,9.2 ± 1.5,and 9.0 ± 1.3,P ＜ 0.05).The content of smooth muscle cells in plaque in CTLA-4Ig group were 11.8 ± 1.0 and higher than those in PBS group,IgG1 group,and blank group (7.8 ± 0.8,7.5 ± 0.9,and 7.3 ± 0.7,P ＜ 0.05).There was no significant difference in content of collagen fibrils and smooth muscle cells between the PBS group,IgG1 group,and blank group (all P ＞ 0.05).[Conclusion] CTLA-4Ig fusion protein could evidently inhibit the atherosclerosis progression and enhance the stability of plaque through increasing the content of collagen fibrils produced by smooth muscle cells intra-plaque in ApoE-/- mice fed on cholesterol diet.

AIM:To study whether hydrogen sulfide (H2S) protects H9c2 cardiomyocytes against high glucose ( HG)-induced injury by inhibiting necroptosis .METHODS:The protein levels of RIP3 ( an indicator of necroptosis ) and cleaved caspase-3 were determined by Western blot .The cell viability was measured by CCK-8 assay.The intracellular le-vels of reactive oxygen species (ROS) were detected by 2’, 7’-dichlorfluorescein diacetate staining followed by photofluo-rography.Mitochondrial membrane potential (MMP) was examined by rhodamine 123 staining followed by photofluorogra-phy.The number of apoptotic cells was observed by Hoechst 33258 nuclear staining followed by photofluorography .RE-SULTS:After the H9c2 cells were treated with HG (35 mmol/L glucose) for 0~24 h, the protein expression of RIP3 in the H9c2 cells was significantly increased at 3 h, 6 h, 9 h, 12 h and 24 h, reaching the maximum level at 24 h.Pretreat-ment of the cells with 400μmol/L NaHS (a donor of H2S) or co-treatment of the cells with necrostatin-1 (Nec-1;a speci-fic inhibitor of necroptosis) considerably blocked the up-regulation of RIP3 protein induced by HG.Moreover, pretreatment with NaHS or co-treatment with Nec-1 obviously inhibited HG-induced injuries , leading to an increase in the cell viability , and decreases in the generation of ROS and MMP loss .On the other hand , pretreatment with NaHS also reduced the num-ber of apoptotic cells and the protein level of cleaved caspase-3 in the HG-treated H9c2 cardiomyocytes .CONCLUSION:H2 S protects H9c2 cardiomyocytes against HG-induced injury by inhibiting necroptosis .

AIM:To investigate the roles of ATP-sensitive potassium ( KATP ) channels in high glucose-induced cardiac injury and the inhibitory effect of hydrogen sulfide ( H2 S) on the cardiomyocyte injury.METHODS:The expres-sion level of KATP channel protein was tested by Western blot.The cell viability was measured by CCK-8 assay.The number of apoptotic cells was observed by Hoechst 33258 nuclear staining.Mitochondrial membrane potential ( MMP) was exam-ined by JC-1 staining.RESULTS:After the H9c2 cells were treated with 35 mmol/L glucose ( high glucose, HG) for 1~24 h, the protein level of KATP channel was significantly reduced at 6 h, 9 h, 12 h and 24 h, reaching the minimum level at 12 h and 24 h.Pretreatment of the cells with 400μmol/L NaHS ( a donor of H2 S) prior to exposure to HG for 12 h con-siderably blocked the down-regulation of KATP channels induced by HG.Pretreatment of the cells with 100 μmol/L mito-chondrial KATP channel opener diazoxide, 50μmol/L non-selective KATP channel opener pinacidil or NaHS obviously inhibi-ted HG-induced injuries, leading to an increase in the cell viability, and decreases in the number of apoptotic cells and the MMP loss.Pretreatment with 100μmol/L mitochondrial KATP channel antagonist 5-hydroxydecanoic acid or 1 mmol/L non-selective KATP channel antagonist glibenclamide attenuated the above cardioprotective effects of NaHS.CONCLUSION:KATP channels mediate the inhibitory effect of H2 S on HG-induced cardiac injury.