Objective : To investigate whether NaHS，a hydrogen sulfide donor，can improve myocardial injury in sepsis by inhibiting oxidative stress and activating the Xc －/ GPX4 signaling pathway in ferroptosis． Methods : Lipopolysacc-haride(LPS) induced H9c2 in rat cardiomyocytes to form an in vitro model of myocardial injury in sep- sis，which was divided into Control group，LPS group and LPS + NaHS group．The kits were applied to detect the changes of cardiomyocyte viability，Fe2 + ，LDH and CK-MB，determine the levels of oxidative stress indexes GSH and MDA，detect the changes of cellular ROS and mitochondrial membrane potential levels by fluorescent probes， and detect the expression levels of ferroptosis regulatory proteins SLC7A11 and GPX4 by Western blot. Results: Compared with the Control group，H9c2 cell viability decreased，Fe2 + concentration increased ，GSH ，MDA and ROS levels increased，mitochondrial JC-1 monomer increased ，expression levels of ferroptosis regulatory proteins SLC7A11 and GPX4 decreased，and cell damage increased after LPS stimulation (P＜0. 05) ．Compared with the LPS group，NaHS attenuated LPS-induced H9c2 cell injury and elevated Fe2 + concentration，decreased the level of LPS-induced oxidative stress in H9c2 cells ，and increased the expression levels of ferroptosis regulatory proteins SLC7A11 and GPX4 (P＜0. 05 ) ． Conclusion The mechanism by which NaHS attenuates myocardial injury in sepsis may be related to the inhibition of oxidative stress and activation of the Xc －/ GPX4 signaling pathway in fer- roptosis.

Objective:To investigate the protective effects and related mechanisms of Astragaloside Ⅳ(ASⅣ)alleviating Angiotensin II-induced cardiomyocyte hypertrophy.Methods:H9c2 cardiomyocytes were divided into six groups: normal control group, ASⅣ group(ASⅣ 100 μmol/L), AngⅡ group(AngⅡ 1 μmol/L), and three ASⅣ dose experiments(AngⅡ 1 μmol/L + ASⅣ 25 μmol/l group, AngⅡ 1 μmol/L+ ASⅣ 50 μmol/l group, AngⅡ1 μmol/L+ ASⅣ 100 μmol/L group), and simultaneously cultured for 24 hours.Cardiomyocyte viability was assessed by CCK8 assay, and surface area of culturedcardiomyocytes in each group was assessed by immunofluorescence assay.Atrial natriuretic peptide(ANP)mRNA expression was assessed by fluorescence real-time quantitative RT-PCR.And LC3 protein expression, an autophagy related protein, was assessed by Western blotting as well as immunofluorescence.Results:(1)AngⅡ decreased cardiomyocyte H9c2 viability in a dose-dependent manner( P<0.05). ASⅣ could inhibit the decrease of cardiomyocyte H9c2 viability in response to AngⅡ in a dose-dependent manner( P<0.05). (2)H9c2 cardiomyocytes induced by AngⅡ showed a significantly larger cell area and significantly higher ANP mRNA and ANP protein expression compared with controls.Different concentrations of ASⅣ intervention could reverse the increase of cardiomyocyte H9c2 area induced by AngⅡ and also decreased the expression of ANP protein induced by AngⅡ in a dose-dependent manner(all P<0.05). (3)Compared with the control group, the autophagy level and the expression of autophagy marker LC3II/I of H9c2 cardiomyocytes induced by AngⅡ were significantly increased(all P<0.05). ASⅣ could inhibit AngⅡ-activated autophagy, and the difference was statistically significant( P<0.05). ASⅣ inhibited the expression of LC3II/I in H9c2 cardiomyocytes stimulated by AngⅡ, and the difference was statistically significant( P<0.05). Conclusions:ASⅣ inhibits AngⅡ-induced cardiac hypertrophy by inhibiting autophagy of cardiomyocytes.

Objective: To explore the application value of closed negative pressure drainage technique in wound healing of hand trauma. Methods: From August 2013 to October 2017, 80 patients with hand trauma in the Traditional Chinese Medicine Hospital of Cixi were divided into two groups according to the random principle, with 40 cases in each group.The control group was treated with conventional wound repair, and the observation group was treated with closed negative pressure drainage.The repair effect, healing, secondary operation, antibiotic use, hospitalization, histopathological score and patients' satisfaction were observed. Results: The total effective rate of the observation group (97.50%) was obviously higher than that of the control group(80.00%)(χ²=6.13, P<0.05). The time of healing, length of hospital stay and the use time of antimicrobial agents in the observation group were (15.11±2.43)d, (16.27±1.79)d and (6.06±0.65)d, respectively, which were all lower than those in the control group(t=14.43, 13.31, 23.29, all P<0.05). The second operation rate of the observation group (5.00%) was lower than that of the control group(P<0.05), and the histopathological score in the observation group (7.11±0.53) was higher than that in the control group(P<0.05). The satisfaction rate of the observation group (100.00%) was obviously higher than that of the control group(χ²=6.49, P<0.05). Conclusion In the treatment of wound healing of hand trauma, the application of closed negative pressure drainage technology is better, which can effectively control the disease and is worthy of further promotion and use.

Objective To construct the eukaryotic expression vector for human hypoxia inducible factor-1? gene (pSNAV-HIF-1?), and to investigate the apoptosis and intracellular calcium concentration of the transfected A?25-35 induced hippocampal neurons of primary culture. Methods Human hypoxia inducible factor-1? gene from pBSKhHIF1?T7 was inserted into pSNAV2.0 by the method of gene recombination, then the constructed vector was transfected into hippocampal neurons of primary culture and followed by A?25-35 for treatment. Empty pSNAV2.0 vector was treated the same way as pSNAV-HIF-1? as a control. The expression level of HIF-1? protein was assayed by Western blotting. Apoptosis was detected by flow cytometry. Intracellular calcium concentration was determined by laser scanning confocal microscopy with Fluo-3/AM as the fluorescent dye. Results It was shown that pSNAV-HIF-1? was successfully constructed by restriction enzyme digestion, PCR and DNA sequencing. The expression level of HIF-1? protein was significantly increased in transfected hippocampal neurons of primary culture (P