Tiwari Prafulla Chandra, Chaudhary Manju J, Pal Rishi, Nath Rajendra
Department of Pharmacology and Therapeutics, King George's Medical University, Lucknow, Uttar Pradesh, India.
Department of Physiology, Government Medical College, Kannauj, Uttar Pradesh, India.
Fundam Clin Pharmacol. 2022 Dec;36(6):944-955. doi: 10.1111/fcp.12817. Epub 2022 Aug 3.
Nitric oxide (NO), generated by nitric oxide synthase enzymes (NOS), has an important role in maintaining synapse plasticity, neuro-modulation, and other physiological functions in the brain. NO thus generated also has a key role in formation of reactive oxygen and reactive nitrite species and subsequent neuronal damage due to sustained oxidative stress. Due to its property of ROS and RNOS generation, NO plays a significant role in Parkinson's disease (PD) pathogenesis. Therefore, we evaluated the effect of mangiferin alone and in combination with nNOS inhibitor 7-nitro-indazole (7-NI) in 6-OHDA lesioned rats. Male Wistar rats weighing 200-250 g (n = 8/group) were used in the study. Stereotactic surgeries of rats were done to induce 6-OHDA lesioning in rats. Then, treatment with mangiferin alone and in combination with 7-NI 10 mg/kg was done from days 14 to 42 for 28 days. On day 42, rats were subjected to behavioral studies, and their brains were taken out after euthanasia to perform biochemical and molecular studies. Treatment with mangiferin and 7-NI significantly increases locomotor parameters in 6-OHDA lesioned rats. Treatment with mangiferin 45 μg and 7-NI 10 mg/kg alone and in combination significantly reduces oxidative stress along with decrease in concentration of pro-inflammatory cytokines, cyclooxygenase 2, total nitrite (NOx) and FOS B concentration. Results of this study suggest that treatment with 7-NI 10 mg/kg further enhances anti-inflammatory and anti-parkinsonism activity of mangiferin owing to its property of inhibiting nNOS mediated FOS B signaling and thereby inhibiting mRNA formation of TNF-α and IL-6.
一氧化氮合酶(NOS)生成的一氧化氮(NO)在维持大脑突触可塑性、神经调节及其他生理功能方面发挥着重要作用。如此生成的NO在活性氧和活性亚硝酸盐的形成以及随后因持续氧化应激导致的神经元损伤中也起着关键作用。由于其具有产生活性氧和活性氮氧化物的特性,NO在帕金森病(PD)发病机制中发挥着重要作用。因此,我们评估了单独使用芒果苷以及将其与nNOS抑制剂7-硝基吲唑(7-NI)联合使用对6-羟基多巴胺(6-OHDA)损伤大鼠的影响。本研究使用了体重200-250 g的雄性Wistar大鼠(每组n = 8)。对大鼠进行立体定向手术以诱导6-OHDA损伤。然后,从第14天至第42天,单独使用芒果苷以及将其与10 mg/kg的7-NI联合使用,持续28天。在第42天,对大鼠进行行为学研究,并在安乐死后取出大脑进行生化和分子研究。芒果苷和7-NI治疗显著提高了6-OHDA损伤大鼠的运动参数。单独使用45 μg芒果苷和10 mg/kg 7-NI以及联合使用均显著降低了氧化应激,同时促炎细胞因子、环氧化酶2、总亚硝酸盐(NOx)和FOS B浓度也有所降低。本研究结果表明,10 mg/kg的7-NI治疗由于其抑制nNOS介导的FOS B信号传导从而抑制TNF-α和IL-6的mRNA形成的特性,进一步增强了芒果苷的抗炎和抗帕金森病活性。