School of Pharmaceutical Sciences, Lovely Professional University, Phagwara, Punjab, 144 411, India; Akal College of Pharmacy and Technical Education, Gursagar Mastuana Sahib, Sangrur, Punjab, 148 001, India; Research Scholar, I.K. Gujral Punjab Technical University, Kapurthala, Punjab, 144 603, India.
School of Pharmaceutical Sciences, Lovely Professional University, Phagwara, Punjab, 144 411, India.
Eur J Pharmacol. 2021 Jul 15;903:174112. doi: 10.1016/j.ejphar.2021.174112. Epub 2021 Apr 24.
In the present study, we investigated the anti-Parkinson's effect of vanillic acid (VA) (12 mg/kg, 25 mg/kg, 50 mg/kg p.o.) against rotenone (2 mg/kg s.c.) induced Parkinson's disease (PD) in rats. The continuous administration of rotenone for 35 days resulted in rigidity in muscles, catalepsy, and decrease in locomotor activity, body weight, and rearing behaviour along with the generation of oxidative stress in the brain (rise in the TBARS, and SAG level and reduced CAT, and GSH levels). Co-treatment of VA and levodopa-carbidopa (100 mg/kg + 25 mg/kg p.o.) lead to a significant (P < 0.001) reduction in the muscle rigidity and catalepsy along with a significant (P < 0.001) increase in body weight, rearing behaviour, locomotion and muscle activity as compared to the rotenone-treated group in the dose dependent manner, showing maximum effect at the 50 mg/kg. It also showed reversal of levels of oxidative stress parameters thus, reducing the neuronal oxidative stress. The level of DA was also estimated which showed an increase in the level of DA in the VA plus standard drug treated animals as compared to rotenone treated group. Histopathological evaluation showed a high number of eosinophilic lesions in the rotenone group which were found to be very less in the VA co-treated group. The study thus proved that co-treatment of VA and levodopa-carbidopa, significantly protected the brain from neuronal damage due to oxidative stress and attenuated the motor defects indicating the possible therapeutic potential of VA as a neuroprotective in PD.
在本研究中,我们研究了香草酸(VA)(12mg/kg、25mg/kg、50mg/kg 口服)对鱼藤酮(2mg/kg 皮下注射)诱导的大鼠帕金森病(PD)的抗帕金森作用。连续给予鱼藤酮 35 天导致肌肉僵硬、僵住和运动活动、体重和后肢行为减少,以及大脑产生氧化应激(TBARS 和 SAG 水平升高,CAT 和 GSH 水平降低)。VA 与左旋多巴-卡比多巴(100mg/kg+25mg/kg 口服)共同治疗导致肌肉僵硬和僵住显著减少(P<0.001),与鱼藤酮处理组相比,体重、后肢行为、运动和肌肉活动显著增加(P<0.001),呈剂量依赖性,在 50mg/kg 时效果最大。它还显示了氧化应激参数水平的逆转,从而减少神经元氧化应激。还评估了 DA 的水平,结果显示,与鱼藤酮处理组相比,VA 加标准药物处理动物的 DA 水平增加。组织病理学评估显示,鱼藤酮组有大量嗜酸性病变,而 VA 共同处理组发现病变非常少。该研究证明,VA 与左旋多巴-卡比多巴的共同治疗显著保护大脑免受氧化应激引起的神经元损伤,并减轻运动缺陷,表明 VA 作为 PD 神经保护剂具有潜在的治疗潜力。