Si Yi-ling, Zhang Jin-ying, Yan Guang-tao
Research Laboratory of Biochemistry, Basic Medical Institute, General Hospital of PLA, Beijing 100853, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2009 Apr;29(4):598-601.
To investigate the protective effect of leptin against cerebral ischemia/reperfusion injury in mice.
Mouse models of transient focal cerebral ischemia were established by occlusion of the right middle cerebral artery for 2 h followed by 24 h reperfusion. The infarct volume and neurological deficit scores following leptin treatment were determined using TTC staining and the Longa's score, respectively, to evaluate the protective effect of leptin against ischemic cerebral injury. The levels of lactate dehydrogenase (LDH), malondialdehyde (MDA) and nitric oxide (NO) in the brain tissue were measured by colorimetry. The histopathological changes in the brain were observed with HE staining, and the expression of glial fibrillary acidicprotein (GFAP) was detected by immunohistochemistry.
Leptin treatment markedly reduced cerebral infarct volume and neurological deficits induced by transient ischemia. The LDH, MDA and NO levels in the brain tissues were significantly decreased after leptin treatment, which also alleviated the histopathological injury, maintained the normal morphology of the astrocytes and increased the expression of GFAP.
Leptin produces obvious protective effect against cerebral ischemia/reperfusion injury by inhibiting lipid peroxidation, stabilizing the internal environment and adjusting the activity of the astrocytes.
探讨瘦素对小鼠脑缺血/再灌注损伤的保护作用。
通过闭塞右侧大脑中动脉2小时,随后再灌注24小时,建立小鼠短暂性局灶性脑缺血模型。分别采用TTC染色和Longa评分法测定瘦素治疗后的梗死体积和神经功能缺损评分,以评估瘦素对缺血性脑损伤的保护作用。采用比色法测定脑组织中乳酸脱氢酶(LDH)、丙二醛(MDA)和一氧化氮(NO)的水平。用HE染色观察脑组织的组织病理学变化,用免疫组织化学法检测胶质纤维酸性蛋白(GFAP)的表达。
瘦素治疗显著减少了短暂性缺血诱导的脑梗死体积和神经功能缺损。瘦素治疗后,脑组织中LDH、MDA和NO水平显著降低,同时减轻了组织病理学损伤,维持了星形胶质细胞的正常形态,并增加了GFAP的表达。
瘦素通过抑制脂质过氧化、稳定内环境和调节星形胶质细胞的活性,对脑缺血/再灌注损伤产生明显的保护作用。