Xu Chao, Zhao Hong-Yan
First Affiliated Hospital, School of Medicine, Shihezi University, Shihezi 832002, China.
Third Affiliated Hospital, School of Medicine, Shihezi University, Shihezi 832003, China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2018 Jul;49(4):540-545.
To study the effects of hydrogen sulfide (H S) on myocardial injury in sepsis rats, and to explore the possible mechanism of H S on myocardial injury induced by sepsis.
Cecal ligation and puncture (CLP) method was used to establish sepsis rat model. SD rats were randomly divided into 6 groups: sham operation group, sham operation + exogenous H S donor sodium thiohydride group, pseudosurgery +H S synthase cthioether-ether lyase (cystathionine-γ-lyase, CSE) inhibitor propargylglycine (propargylglycine, PAG) group, CLP model group, CLP model +NaHS group, CLP model +PAG group, 24 rats in each group. Blood and myocardial specimens were collected from the subgroups of COP for 6 h, 12 h and 24 h, respectively. Serum myocardial calcitonin I (cTnI) level, TNF-α, IL-10 were detected, and the pathological changes were observed by HE staining of rat myocardial tissue. The expression of mRNA in cardiomyocytes was detected by RT-PCR, Western blot assay was used to detect the expression of cardiac transcription factor NF-κB in rats.
There was no statistically significant difference in each group and time point of sham operation groups. Compared to the sham 12 h, 24 h group, the concentration of cTnI in serum, and pathological scores of myocardial tissue increased gradually (<0.05) in the CLP 12 h and 24 h group. Compared to the CLP 12 h, 24 h group, in the CLP + NaHS 12 h, 24 h group, the concentration of cTnI in serum, and pathological scores of myocardial tissue, the expression of NF-κB, the level of TNF-α decreased and the expression of mRNA and the level of IL-10 increased (<0.05); in the CLP + PAG 12 h, 24 h group, the concentration of cTnI in serum, and pathological scores of myocardial tissue, the expression of NF-κB, the level of TNF-α increased gradually (<0.05); and the expression of mRNA and the level of IL-10 increased (<0.05).
H S plays a protective role in sepsis-induced myocardial injury, and the possible mechanism of this protective effect maybe by inhibiting the expression of NF-κB, reducing the content of TNF-α and improving the content of IL-10 in myocardial tissue.
研究硫化氢（H₂S）对脓毒症大鼠心肌损伤的影响，探讨H₂S对脓毒症所致心肌损伤的可能机制。
采用盲肠结扎穿孔（CLP）法建立脓毒症大鼠模型。将SD大鼠随机分为6组：假手术组、假手术+外源性H₂S供体硫代硫酸钠组、假手术+H₂S合酶胱硫醚-γ-裂解酶（cystathionine-γ-lyase，CSE）抑制剂炔丙基甘氨酸（propargylglycine，PAG）组、CLP模型组、CLP模型+NaHS组、CLP模型+PAG组，每组24只大鼠。分别于术后6 h、12 h和24 h从各亚组采集血液和心肌标本。检测血清心肌肌钙蛋白I（cTnI）水平、TNF-α、IL-10，并通过大鼠心肌组织HE染色观察病理变化。采用RT-PCR检测心肌细胞中mRNA的表达，Western blot法检测大鼠心脏转录因子NF-κB的表达。
假手术组各时间点组间比较差异无统计学意义。与假手术12 h、24 h组比较，CLP 12 h和24 h组血清cTnI浓度及心肌组织病理评分逐渐升高（P<0.05）。与CLP 12 h、24 h组比较，CLP+NaHS 12 h、24 h组血清cTnI浓度、心肌组织病理评分、NF-κB表达、TNF-α水平降低，mRNA表达及IL-10水平升高（P<0.05）；CLP+PAG 12 h、24 h组血清cTnI浓度、心肌组织病理评分、NF-κB表达、TNF-α水平逐渐升高（P<0.05）；mRNA表达及IL-10水平升高（P<0.05）。
H₂S对脓毒症所致心肌损伤具有保护作用，其保护作用的可能机制是通过抑制NF-κB表达、降低心肌组织中TNF-α含量、提高IL-10含量。
