Yaidikar Lavanya, Thakur Santhrani
Division of Pharmacology, Institute of Pharmaceutical Technology, Sri Padmavati Mahila Visvavidyalayam (Women's University), Tirupati, India.
Division of Pharmacology, Institute of Pharmaceutical Technology, Sri Padmavati Mahila Visvavidyalayam (Women's University), Tirupati, India.
Pharmacol Rep. 2015 Oct;67(5):890-5. doi: 10.1016/j.pharep.2015.02.003. Epub 2015 Feb 19.
Arjunolic acid (AA), a pentacyclic triterpenoidal saponin of Terminalia arjuna is well recognized for its antioxidant properties. We proposed to evaluate its antioxidant potential against focal cerebral ischemia reperfusion (I/R) injury in rats subjected to middle cerebral artery occlusion (MCAO).
In the present study, rats were randomly divided into a sham, MCAO, AA (10 and 20mg/kg) treated groups. Rats received their respective treatment orally by gavage for 7 days prior to MCAO. Rats were anaesthetized with ketamine (100mg/kg), xylazine (10mg/kg) and subjected to 2h occlusion and 22h reperfusion. Neurological deficit, brain water content and oxidative stress markers were measured after 22h of reperfusion.
Rats pretreated with AA showed significantly reduced neurological deficit score, infarct size. AA prevented neuronal damage induced by I/R by regulating the levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO), protein carbonyl content and mitochondria generated reactive oxygen species. In addition, it also controlled the enzyme activities of Na(+)-K(+) ATPase, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR).
Pre-treatment with AA effectively prevented the cerebral I/R induced oxidative damage by virtue of its antioxidant potential. These results indicate that supplementation of AA may be beneficial in stroke prone population.
阿朱诺酸(AA)是诃子中的一种五环三萜皂苷,其抗氧化特性已得到广泛认可。我们旨在评估其对大脑中动脉闭塞(MCAO)大鼠局灶性脑缺血再灌注(I/R)损伤的抗氧化潜力。
在本研究中,大鼠被随机分为假手术组、MCAO组、AA(10和20mg/kg)治疗组。在MCAO前7天,大鼠通过灌胃口服各自的治疗药物。大鼠用氯胺酮(100mg/kg)、赛拉嗪(10mg/kg)麻醉,进行2小时闭塞和22小时再灌注。再灌注22小时后测量神经功能缺损、脑含水量和氧化应激标志物。
用AA预处理的大鼠神经功能缺损评分、梗死面积显著降低。AA通过调节丙二醛(MDA)、还原型谷胱甘肽(GSH)、一氧化氮(NO)、蛋白质羰基含量和线粒体产生的活性氧水平,预防了I/R诱导的神经元损伤。此外,它还控制了钠钾ATP酶、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)和谷胱甘肽还原酶(GR)的酶活性。
AA预处理凭借其抗氧化潜力有效预防了脑I/R诱导的氧化损伤。这些结果表明,补充AA可能对易患中风的人群有益。