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慢性间歇性低氧暴露小鼠心肌细胞损伤中氧化应激的作用。

The effect of oxidative stress in myocardial cell injury in mice exposed to chronic intermittent hypoxia.

机构信息

Department of Respiratory Diseases, Jiangsu Geriatric Hospital, Nanjing, Jiangsu 210024, China.

出版信息

Chin Med J (Engl). 2010 Jan 5;123(1):74-8.

PMID:20137579
Abstract

BACKGROUND

Obstructive sleep apnea syndrome (OSAS) is an important risk factor for cardiovascular diseases. Chronic intermittent hypoxia (CIH) is considered to be one of the most important causes of cardiovascular diseases in OSA patients. This repeated hypoxia and reoxygenation cycle is similar to hypoxia-reperfusion injury, which initiates oxidative stress. In this study, we observed cardiocytes injury induced by CIH and the effect of N-acetylcysteine (NAC).

METHODS

Thirty ICR mice were randomly assigned to 3 groups: control, CIH and NAC (CIH + NAC) groups. Malondialdehyde (MDA) and superoxide dismutase (SOD) of cardiocyte homogenates were measured. Serum lipids were measured by an instrument method. Serum cardiac troponin I (cTnI) was detected by enzyme-linked immunosorbent assays (ELISA). Myocardium pathological sections were observed.

RESULTS

(1) The SOD activity and MDA concentration of cardiocyte homogenates in the CIH group were significantly higher than in other groups (P < 0.005). The MDA concentration of the NAC group was lower than that of the control group (P < 0.01). (2) The serum cTnI concentration of the CIH and NAC groups was significantly higher than that of the control group (P < 0.01). (3) Serum triglyceride levels in the NAC group were lower than in the other groups (P < 0.01), while there were no significant differences in low density lipoprotein and high density lipoprotein among the three groups. (4) The degeneration of myocardium, transverse striation blurred, and fabric effusion were observed in tissue sections in the CIH and NAC groups. However, normal tissue was found in the control group.

CONCLUSION

The oxidative stress induced by CIH can injure cardiocytes and the injury effect can be partially inhibited by NAC.

摘要

背景

阻塞性睡眠呼吸暂停综合征(OSAS)是心血管疾病的重要危险因素。慢性间歇性低氧(CIH)被认为是 OSA 患者心血管疾病的最重要原因之一。这种反复的缺氧和再氧合循环类似于缺氧再灌注损伤,引发氧化应激。在本研究中,我们观察了 CIH 诱导的心肌细胞损伤及 N-乙酰半胱氨酸(NAC)的作用。

方法

将 30 只 ICR 小鼠随机分为 3 组:对照组、CIH 组和 NAC(CIH+NAC)组。测量心肌细胞匀浆中的丙二醛(MDA)和超氧化物歧化酶(SOD)。仪器法测量血清脂质。酶联免疫吸附试验(ELISA)检测血清心肌肌钙蛋白 I(cTnI)。观察心肌病理切片。

结果

(1)CIH 组心肌细胞匀浆中 SOD 活性和 MDA 浓度明显高于其他组(P<0.005),NAC 组 MDA 浓度低于对照组(P<0.01)。(2)CIH 和 NAC 组血清 cTnI 浓度明显高于对照组(P<0.01)。(3)NAC 组血清三酰甘油水平低于其他两组(P<0.01),而三组间低密度脂蛋白和高密度脂蛋白无显著差异。(4)组织切片中可见 CIH 和 NAC 组心肌变性、横纹模糊、间质渗出,而对照组组织正常。

结论

CIH 诱导的氧化应激可损伤心肌细胞,NAC 可部分抑制损伤作用。

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