Mojtaba Karimipour1, Sara Shojaei Zarghani2, Majid Mohajer Milani3, Hamid Soraya2,3. 1. Neurophysiology Research Center, Department of Anatomy, Urmia University of Medical Sciences, Urmia, Iran. 2. Cellular and Molecular Research Center, Urmia University of Medical Sciences, Urmia, Iran. 3. Department of Pharmacology, Urmia University of Medical Sciences, Urmia, Iran.
Abstract
OBJECTIVE: To explore the effects of pre versus post ischemic treatment with metformin after global cerebral ischemia in rats. METHODS: Male Wister rats underwent forebrain ischemia by bilateral common carotid artery occlusion for 17 min. Metformin (200 mg/kg) or vehicle was given orally by gavage for 7-14 days. Rats were divided into: control, metformin pre-treatment, metformin post-treatment and metformin pre and post continuous treatment groups. Cerebral infarct size, histopathology, myeloperoxidase and serum malondialdehyde were measured 7 days after ischemia. RESULTS: Histopathological analysis showed that metformin pre-treatment significantly decreased leukocyte infiltration, myeloperoxidase activity and also malondialdehyde level. Metformin pre-treatment and metformin post-treatment reduced infarct size compared with the control group, but it was not significant in the pre and post continuous treatment group. CONCLUSION: Our findings suggest that pre-treatment with metformin in comparison with post-treatment in experimental stroke can reduce the extent of brain damage and is more neuroprotective at least in part by inhibiting oxidative stress and inflammation.
OBJECTIVE: To explore the effects of pre versus post ischemic treatment with metformin after global cerebral ischemia in rats. METHODS: Male Wister rats underwent forebrain ischemia by bilateral common carotid artery occlusion for 17 min. Metformin (200 mg/kg) or vehicle was given orally by gavage for 7-14 days. Rats were divided into: control, metformin pre-treatment, metformin post-treatment and metformin pre and post continuous treatment groups. Cerebral infarct size, histopathology, myeloperoxidase and serum malondialdehyde were measured 7 days after ischemia. RESULTS: Histopathological analysis showed that metformin pre-treatment significantly decreased leukocyte infiltration, myeloperoxidase activity and also malondialdehyde level. Metformin pre-treatment and metformin post-treatment reduced infarct size compared with the control group, but it was not significant in the pre and post continuous treatment group. CONCLUSION: Our findings suggest that pre-treatment with metformin in comparison with post-treatment in experimental stroke can reduce the extent of brain damage and is more neuroprotective at least in part by inhibiting oxidative stress and inflammation.
Entities:
Keywords:
Global cerebral ischemia; Inflammation.; Metformin; Oxidative stress
Authors: Tobias M Huijink; Leonie H Venema; Rene A Posma; Nynke J de Vries; Andrie C Westerkamp; Petra J Ottens; Daan J Touw; Maarten W Nijsten; Henri G D Leuvenink Journal: Clin Transl Sci Date: 2020-07-31 Impact factor: 4.689