Praveen Kumar P, D Madhuri, Siva Sankar Reddy L, Dastagiri Reddy Y, Somasekhar G, Sirisha N V L, Nagaraju K, Shouib M S, Rizwaan A S
Santhiram College of Pharmacy, Nandyal, Kurnool, Andhra Pradesh, India.
Creative Educational Societys College of Pharmacy, Kurnool, Andhra Pradesh, India.
Saudi J Biol Sci. 2021 Sep;28(9):5204-5213. doi: 10.1016/j.sjbs.2021.05.044. Epub 2021 May 24.
Current study was designed multiple occlusions and reperfusion of bilateral carotid arteries induced cerebral injury model and evaluated the protective effect of gallic acid on it. study was involved to study gallic acid binding affinity on cerebrotonic proteins compared with standard drugs using . Cerebral ischemia was induced by occlusion of bilateral common carotid arteries for 10 mins followed by 10 reperfusions (1 cycle), cycle was continued to 3 cycles (MO/RCA), then pathological changes were observed by estimation of brain antioxidants as superoxide dismutase, glutathione, catalase, oxidants like malonaldehyde, cerebral infarction area, histopathology, and study gallic acid treatment against cerebral injury. Gallic acid exhibited a strong binding affinity on targeted cerebrotoxic proteins. MO/RCA rat brain antioxidant levels were significantly decreased and increased MDA levels (p < 0.0001), Infarction size compared to sham rats. Gallic acid treatment rat brain MDA levels significantly decreased (p < 0.4476) and increased SOD (p < 0.0001), CAT (p < 0.0001), GSH (p < 0.0001), cerebral infarction area when compared to MO/RCA group. Developed model showed significant cerebral ischemic injury in rats, injury was ameliorated by Gallic acid treatment and in silico approaches also inhibit the cerebrotoxic protein function by targeting on active sites.
本研究设计了双侧颈动脉多次闭塞和再灌注诱导的脑损伤模型,并评估了没食子酸对其的保护作用。该研究还涉及与标准药物相比,研究没食子酸对脑增强蛋白的结合亲和力。通过双侧颈总动脉闭塞10分钟,然后进行10次再灌注(1个循环)来诱导脑缺血,该循环持续至3个循环(MO/RCA),然后通过评估脑抗氧化剂如超氧化物歧化酶、谷胱甘肽、过氧化氢酶、氧化剂如丙二醛、脑梗死面积、组织病理学来观察病理变化,并研究没食子酸对脑损伤的治疗作用。没食子酸对靶向脑毒性蛋白表现出很强的结合亲和力。与假手术组大鼠相比,MO/RCA大鼠脑抗氧化剂水平显著降低,丙二醛水平升高(p<0.0001),梗死面积增大。与MO/RCA组相比,没食子酸治疗的大鼠脑丙二醛水平显著降低(p<0.4476),超氧化物歧化酶(p<0.0001)、过氧化氢酶(p<0.0001)、谷胱甘肽(p<0.0001)水平升高,脑梗死面积减小。所建立的模型显示大鼠存在明显的脑缺血损伤,没食子酸治疗可改善损伤,并且计算机模拟方法也通过靶向活性位点抑制脑毒性蛋白的功能。