Original Research Article
Year: 2021 | Month: October | Volume: 8 | Issue: 10 | Pages: 242-247
DOI: https://doi.org/10.52403/ijrr.20211031
Experimental Brain Injury Induced by Acute Hypobaric Hypoxia Stimulates Changes in mRNA Expression and Stress Marker Status
Muhammad Shoaib Tahir1, 2, Maged Almezgagi1, 2, Yu Zhang2, Du Zhonglei2, Zhu Qinfang2, Muhammad Ali3, Zaid Shouket4,Wei Zhang1, 2
1The Key Laboratory of High-Altitude Medical Application of Qinghai Province, Qinghai University, Qinghai Xining 810001, China.
2Department of Basic Medicine, Medical College of Qinghai University, Qinghai Xining 810001, China.
3Northern Jiangsu People’s Hospital, Medical College of Yangzhou University, Yangzhou 225001, China.
4Department of General Surgery, Xinjiang Medical University First Affiliated Hospital, Xinjiang Urumqi 830054, China.
Corresponding Author: Wei Zhang
ABSTRACT
The present study was proposed to investigate the brain injury under acute hypobaric hypoxia following alteration in mRNA expression and stress markers in a time-dependent manner. SD clean graded male rats were randomly divided into four groups for this experimental brain injury, the control group at Xining (altitude, 2270m) and hypoxia treatment groups with different time exposure day1, day2, and day3 at (altitude, 7000m) in a hypobaric chamber. After day3 exposure, the brain tissues were collected. The level of mRNA expression of VEGF and HIF1-α was assessed using qRT-PCR. The oxidative stress level of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined with commercial kits. AHH with time duration significantly increased the MDA level and decreased in the activity of SOD was seen in all hypoxia treated groups as compared to the control (P< 0.001). The mRNA expression level of HIF1-α and VEGF in day1, day2, and day3 AHH groups was markedly raised when it is compared to control (P< 0.05). Ultimately, in conclusion, such results indicate that AHH stimulates oxidative stress induces brain damage in rats.
Keywords: Acute hypobaric hypoxia, Brain injury, HIF-1α, Oxidative stress.
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