Swathy S S, Indira M
Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram - 695 581, Kerala, India.
Int J Ayurveda Res. 2010 Jan;1(1):4-9. doi: 10.4103/0974-7788.59936.
One of the mechanisms of neurotoxicity is the induction of oxidative stress. There is hardly any cure for neurotoxicity in modern medicine, whereas many drugs in Ayurveda possess neuroprotective effects; however, there is no scientific validation for these drugs. Ksheerabala is an ayurvedic drug which is used to treat central nervous system disorders, arthritis, and insomnia. The aim of our study was to evaluate the effect of Ksheerabala on quinolinic acid-induced toxicity in rat brain. The optimal dose of Ksheerabala was found from a dose escalation study, wherein it was found that Ksheerabala showed maximum protection against quinolinic acid-induced neurotoxicity at a dose of 15 microL/100 g body weight/day, which was selected for further experiments. Four groups of female albino rats were maintained for 21 days as follows: 1. Control group, 2. Quinolinic acid (55 microg/100 g body weight), 3. Ksheerabala (15 microL/100 g body weight), 4. Ksheerabala (15 microL/100 g body weight) + Quinolinic acid (55 microg/100 g body weight). At the end of the experimental period, levels of lipid peroxidation products, protein carbonyls, and activities of scavenging enzymes were analyzed. The results revealed that quinolinic acid intake caused enhanced lipid and protein peroxidation as evidenced by increased levels of peroxidation products such as malondialdehyde, hydroperoxide, conjugated dienes, and protein carbonyls. On the other hand, the activities of scavenging enzymes such as catalase, superoxide dismutase (SOD), glutathione peroxidase, and glutathione reductase as well as the concentration of glutathione were reduced. On coadminstration of Ksheerabala along with quinolinic acid, the levels of all the biochemical parameters were restored to near-normal levels, indicating the protective effect of the drug. These results were reinforced by histopathological studies.
神经毒性的机制之一是诱导氧化应激。现代医学中几乎没有治疗神经毒性的方法,而阿育吠陀医学中的许多药物具有神经保护作用;然而,这些药物尚未得到科学验证。Ksheerabala是一种用于治疗中枢神经系统疾病、关节炎和失眠的阿育吠陀药物。我们研究的目的是评估Ksheerabala对喹啉酸诱导的大鼠脑毒性的影响。通过剂量递增研究确定了Ksheerabala的最佳剂量,结果发现Ksheerabala在剂量为15微升/100克体重/天时对喹啉酸诱导的神经毒性具有最大保护作用,该剂量被选用于进一步实验。将四组雌性白化大鼠饲养21天,分组如下:1. 对照组,2. 喹啉酸(55微克/100克体重),3. Ksheerabala(15微升/100克体重),4. Ksheerabala(15微升/100克体重)+喹啉酸(55微克/100克体重)。在实验期结束时,分析脂质过氧化产物、蛋白质羰基水平以及清除酶的活性。结果显示,摄入喹啉酸导致脂质和蛋白质过氧化增强,丙二醛、氢过氧化物、共轭二烯和蛋白质羰基等过氧化产物水平升高证明了这一点。另一方面,过氧化氢酶、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶和谷胱甘肽还原酶等清除酶的活性以及谷胱甘肽的浓度降低。Ksheerabala与喹啉酸共同给药时,所有生化参数水平恢复到接近正常水平,表明该药物具有保护作用。组织病理学研究进一步证实了这些结果。