Chen Wen, Liu Ning, Zhang Ying, Qi Yingchun, Yang Jing, Deng Zhaoyang, Li Xiaoling, Xie Xiaohua
Department Geriatric General Surgery, General Hospital of PLA, Beijing 100853, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2013 Apr;33(4):554-8.
To assess the protective effect of exogenous hydrogen sulfide (H₂S) against myocardial injury after skeletal muscle ischemia/reperfusion (IR) in rats and explore the mechanism.
Thirty-one Wistar rats were randomized into normal control (n=8), IR group (n=8, with a 4-h reperfusion following a 4-h ischemia of the bilateral hindlimbs induced using a tourniquet), NaHS group (n=8, with IR and intraperitoneal injection of 14 µmol/kg NaHS), and DL-propargylglycine (PPG) group (n=7, with IR and intraperitoneal injection of 50 mg/kg PPG). The plasma levels of CK-MB and the levels of MPO, TNF-α, MDA, T-SOD, and CuZn-SOD in the plasma and myocardial tissues were measured. The expression of TNF-α in the myocardium was examined using immunohistochemistry. RESULTS Skeletal muscle IR induced significantly increased plasma CK-MB level (P<0.05) and the levels of MPO, TNF-α, and MDA in the plasma and myocardium, and significantly decreased plasma and myocardial levels of T-SOD and CuZn-SOD (P<0.05). NaHS treatment significantly decreased plasma CK-MB level (P<0.05), reduced plasma and myocardial levels of MPO, TNF-α, and MDA, and increased plasma and myocardial T-SOD and CuZn-SOD in rats with IR (P<0.05), whereas PPG treatment did not produce any obvious responses (P>0.05). Immunohistochemistry showed an obviously reduced expression of TNF-α in the myocardium in rats with NaHS treatment compared with those in IR group.
H₂S treatment can alleviate myocardial injury induced by skeletal muscle IR in rats by inhibiting the inflammatory cytokines and oxidative stress.
评估外源性硫化氢（H₂S）对大鼠骨骼肌缺血/再灌注（IR）后心肌损伤的保护作用并探讨其机制。
将31只Wistar大鼠随机分为正常对照组（n = 8）、IR组（n = 8，使用止血带诱导双侧后肢缺血4小时后再灌注4小时）、NaHS组（n = 8，IR并腹腔注射14 μmol/kg NaHS）和DL-炔丙基甘氨酸（PPG）组（n = 7，IR并腹腔注射50 mg/kg PPG）。检测血浆肌酸激酶同工酶（CK-MB）水平以及血浆和心肌组织中髓过氧化物酶（MPO）、肿瘤坏死因子-α（TNF-α）、丙二醛（MDA）、总超氧化物歧化酶（T-SOD）和铜锌超氧化物歧化酶（CuZn-SOD）的水平。采用免疫组织化学法检测心肌中TNF-α的表达。结果骨骼肌IR导致血浆CK-MB水平显著升高（P < 0.05），血浆和心肌中MPO、TNF-α和MDA水平显著升高，血浆和心肌中T-SOD和CuZn-SOD水平显著降低（P < 0.05）。NaHS治疗显著降低了IR大鼠的血浆CK-MB水平（P < 0.05），降低了血浆和心肌中MPO、TNF-α和MDA水平，并升高了血浆和心肌中T-SOD和CuZn-SOD水平（P < 0.05），而PPG治疗未产生明显反应（P > 0.05）。免疫组织化学显示，与IR组相比，NaHS治疗的大鼠心肌中TNF-α表达明显降低。
H₂S治疗可通过抑制炎性细胞因子和氧化应激减轻大鼠骨骼肌IR诱导的心肌损伤。
