College of Pharmacy, Nanjing University of Chinese Medicine, 282 Hanzhong Road, Nanjing, Jiangsu, China.
Am J Chin Med. 2011;39(2):325-33. doi: 10.1142/S0192415X11008853.
The present study aimed to investigate the protective effects of injectable caltrop fruit saponin preparation (ICFSP) on ischemia-reperfusion injury in rat brain. Rats were injected with ICFSP and then subjected to cerebral ischemia-reperfusion injury induced by middle cerebral artery occlusion. Then the neurological deficit score was evaluated by Bederson's method. The infarct size was assessed by TTC staining. The content of malondialdehyde (MDA) and nitric oxide (NO), and the activity of superoxide dismutase (SOD) in rat cerebrum were measured with kits, and the content of 6 K prostaglandin F1α (6-K-PGF 1α), thromboxane B2 (TXB2) and endothelin (ET) in blood plasma was measured by radioimmunoassay. The results demonstrated that ICFSP led to a decrease in infarct size (p < 0.01), neurological deficit score (p < 0.05) and plasma content of TXB2 and ET (p < 0.05), and an increase of the plasma level of 6-K-PGF 1α (p < 0.05) and SOD activity in cerebrum, where the MDA and NO content were decreased. The treatment improved forelimb function. ICFSP showed a similar potency compared to that of Ligustrazine hydrochloride parenteral solution (LHPS) and nimodipine (Nim). We concluded that ICFSP protects the brain damage caused by ischemia-reperfusion injury in rats, and this may be closely related to the regulation of reactive oxygen species (MDA and SOD activity) and NO levels in the rat cerebrum, as well as vasoactive factors in the plasma (6-K-PGF 1α, TXB2 and ET).
本研究旨在探讨注射用杠柳总皂苷(ICFSP)对大鼠脑缺血再灌注损伤的保护作用。大鼠给予 ICFSP 后,通过大脑中动脉闭塞诱导脑缺血再灌注损伤,然后采用 Bederson 法评估神经功能缺损评分。采用 TTC 染色评估梗死面积。试剂盒测定大鼠脑组织丙二醛(MDA)和一氧化氮(NO)含量及超氧化物歧化酶(SOD)活性,放射免疫法测定血浆 6-酮前列腺素 F1α(6-K-PGF1α)、血栓素 B2(TXB2)和内皮素(ET)含量。结果表明,ICFSP 可降低梗死面积(p<0.01)、神经功能缺损评分(p<0.05)和血浆 TXB2 和 ET 含量(p<0.05),增加血浆 6-K-PGF1α 水平(p<0.05)和大脑 SOD 活性,降低 MDA 和 NO 含量。治疗改善了前肢功能。ICFSP 的作用与盐酸川芎嗪注射液(LHPS)和尼莫地平(Nim)相似。我们得出结论,ICFSP 可保护大鼠脑缺血再灌注损伤引起的脑损伤,这可能与调节大脑中的活性氧物质(MDA 和 SOD 活性)和 NO 水平以及血浆中的血管活性因子(6-K-PGF1α、TXB2 和 ET)密切相关。