A new cerebral ischemic injury model in rats, preventive effect of gallic acid and in silico approaches

• Published in: Saudi journal of biological sciences Vol. 28; no. 9; pp. 5204 - 5213
• Main Authors: 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.
• Format: Journal Article
• Language: English
• Published: Riyadh, Saudi Arabia Elsevier B.V 01.09.2021; Saudi Biological Society; Elsevier
• Subjects: Antioxidants; GA (Gallic acid); In silico; Inflammatory mediators; Multiple occlusion-reperfusion of bilateral common carotid arteries (MO/RCA); Original; Antioxidants; In silico; GA (Gallic acid); Inflammatory mediators; Multiple occlusion-reperfusion of bilateral common carotid arteries (MO/RCA)
• ISSN: 1319-562X; 2213-7106
• DOI: 10.1016/j.sjbs.2021.05.044

[Display omitted] 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. In silico study was involved to study gallic acid binding affinity on cerebrotonic proteins compared with standard drugs using Autodoc vina tool. 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.