[1]陈雯,刘宁,张颖,等.硫化氢通过抑制炎性细胞因子及氧化应激保护大鼠骨骼肌缺血再灌注的心肌损伤[J].南方医科大学学报,2013,(04):554.
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硫化氢通过抑制炎性细胞因子及氧化应激保护大鼠骨骼肌缺血再灌注的心肌损伤()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2013年04期
页码:
554
栏目:
出版日期:
2013-04-15

文章信息/Info

作者:
陈雯刘宁张颖齐迎春杨靖邓昭阳李晓玲谢晓华
关键词:
骨骼肌缺血再灌注心肌损伤硫化氢炎性细胞因子氧化应激
Keywords:
skeletal muscle ischemia/reperfusion myocardial injury hydrogen sulfide inflammatory cytokine oxidative stress
摘要:
目的研究外源性硫化氢对大鼠骨骼肌缺血再灌注的炎性细胞因子和氧化应激的影响,探讨其对骨骼肌缺血再灌注后心
肌损伤的具体保护机制。方法雄性Wistar 大鼠31 只,随机分为4 组①正常对照组(c 组,8 只);②缺血再灌注组(ischemia
reperfusion, IR组,8只):应用止血带结扎双下肢构建大鼠骨骼肌缺血再灌注模型,缺血4 h再灌注4 h;③NaHS组(8只)和PPG
组(7 只):在上述骨骼肌缺血再灌注的模型中,分别于缺血前及再灌注前腹腔注射NaHS 14 μmol/kg、炔丙基甘氨酸(PPG)
50 mg/kg。观察4 组大鼠心肌组织病理、肌酸激酶同工酶(CK-MB)以及血浆和心肌髓过氧化物酶(MPO)、肿瘤坏死因子-α
(TNF-α)、丙二醛(MDA)、超氧化物歧化酶(T-SOD、CuZn-SOD)的变化。以免疫组化法观察心肌细胞TNF-α的表达。结果与c
组比较,IR组血浆CK-MB明显上升,血浆及心肌MPO、MDA水平明显上升,T-SOD、CuZn-SOD水平明显下降(P<0.05),与IR
组比较,NaHS干预后血浆CK-MB明显降低,同时,血浆及心肌MPO、MDA水平明显下降,T-SOD、CuZn-SOD水平明显上升
(P<0.05);PPG组上述指标同IR组没有明显改变(P>0.05)。心肌TNF-α免疫组化可见IR组心肌胞浆棕色染色颗粒较正常对照
组明显增多,NaHS干预后后心肌胞浆棕色染色颗粒明显减少。结论给予H2S的供体NaHS可以通过降低中性粒细胞浸润及前
炎症细胞因子激活、抑制氧化应激反应对骨骼肌缺血再灌注的心肌损伤发挥保护作用。
Abstract:
Objective 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. Methods 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. Conclusion H2S treatment can alleviate myocardial injury induced by
skeletal muscle IR in rats by inhibiting the inflammatory cytokines and oxidative stress.

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更新日期/Last Update: 1900-01-01