Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Effect of oxymatrine on hypoxic-ischemic brain injury in neonatal rats

Chao Wei¹, Shujing Zhao², Ruiqing Diao², Liang He³, Weizhan Wang⁴, Aihuan Li⁴

¹Department One Ward of Neurosurgery, Zhuji People's Hospital of Zhejiang Province, Zhuji People's Hospital Affiliated to Shaoxing University of Arts and Sciences, Zhuji 311800, Zhejiang Province; ²Department of Neurology, Gucheng County Hospital of Hebei Province, Hengshui 253800, Hebei Province; ³Department of Ophthalmology, Hengshui Second People's Hospital, Hengshui 053000, Hebei Province; ⁴Department of Emergency Medicine, Hudson International Peace Hospital affiliated to Hebei Medical University, Hengshui 053000, Hebei Province, China.

For correspondence:- Aihuan Li Email: tcdvb4@163.com

Accepted: 25 May 2021 Published: 30 June 2021

Citation: Wei C, Zhao S, Diao R, He L, Wang W, Li A. Effect of oxymatrine on hypoxic-ischemic brain injury in neonatal rats. Trop J Pharm Res 2021; 20(6):1211-1216 doi: 10.4314/tjpr.v20i6.17

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To study the influence of oxymatrine on hypoxic-ischemic brain injury (HIBI) in neonatal rats.

Methods: Newborn SPF Sprague-Dawley (SD) rats were randomly assigned to 3 groups (10 rats/group): control, HIBI and oxymatrine groups. Neurobehavioral latency of each rat was determined after 48 h of treatment, and pathological changes in rat cerebral cortex were evaluated using H&E staining. Hippocampal neurons prepared from rat brain tissue were grouped and treated as per the above in vivo study. Cell survival and neuronal apoptotic changes were measured with CCK-8 and flow cytometric analysis, respectively, while protein expressions of bcl-2, mcl-1, bax, caspase-3, PI3K, p-PI3K, Akt, p-Akt, GSK3β and p-GSK3β were determined with Western blotting.

Results: Treatment of HIBI rats with oxymatrine significantly reduced their neurobehavioral latencies (reflex, cliff avoidance reflex, and negative reflex (latencies), but repaired HIBI-induced histological damage in rat cerebral cortex (p < 0.05). It also significantly enhanced the survival of rat hippocampal neurons, while reducing neuronal apoptosis (p < 0.05). Moreover, oxymatrine significantly upregulated bcl-2, mcl-1, p-PI3K, AKT, p-AKT, GSK3β and p-GSK3β protein expressions, but i significantly downregulated the protein expressions of bax and caspase-3 in cerebral cortex of HIBI rat (p < 0.05).

Conclusion: These results indicate that oxymatrine reduces neuronal apoptosis and alleviates HIBI in rats via the regulation of proteins associated with PI3K/Akt/GSK3β signal pathway. This finding provides a new research direction on novel botanical monomers for treating HIBI

Keywords: Cell survival, Hypoxic-ischemic brain injury, Neurobehavioral latency, Neuronal apoptosis, Oxymatrine