Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Protective effect of luteolin against oxidative stress during hypoxic ischemia-induced neuronal damage in neonatal rats

Weihong Cao, Jun Luo, Jingwei Peng, Xiaoxia Zhu, Shigang Li, Jilong Ma

Department of Paediatrics, Affiliated Renhe Hospital of China Three Gorges University, Yichang, Hubei, China;

For correspondence:- Jilong Ma Email: jilongma1986@hotmail.com Tel:+867176554671

Accepted: 21 March 2021 Published: 30 April 2021

Citation: Cao W, Luo J, Peng J, Zhu X, Li S, Ma J. Protective effect of luteolin against oxidative stress during hypoxic ischemia-induced neuronal damage in neonatal rats. Trop J Pharm Res 2021; 20(4):749-755 doi: 10.4314/tjpr.v20i4.13

© 2021 The authors.
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Abstract

Purpose: To investigate the neuroprotective efficacy of plant polyphenol luteolin against hypoxic ischemia (HI)-induced neuronal injury in neonatal rat pups.

Methods: Postnatal rat pups (aged 7 days) were subjected to HI insult, and then treated with luteolin at a dose of 1.2 mg/kg body weight (bwt) for up to 4 days after HI injury. Following the sacrifice of the pups, the brain tissues were subjected to histological examination (H & E staining), as well as biochemical and antioxidant assays. Moreover, levels of cell death regulator proteins were determined by enzyme-linked immunosorbent assay (ELISA).

Results: There was significant increase in the tissue levels of reactive oxygen species (ROS) and malondialdehyde (MDA), but marked decrease in mitochondrial membrane potential (ΔΨm) in the HI rat pups (p < 0.05). Furthermore, HI decreased the brain tissue levels of the antioxidants, SOD, CAT, GPX and GSH, in the postnatal pups. However, luteolin treatment significantly reversed the abnormal increase in the levels of ROS and MDA, but reduced the loss in mitochondrial membrane potential (ΔΨm), while increasing the levels of SOD, CAT GPX and GSH (p < 0.05). Furthermore, HI significantly increased the brain expression levels of the pro-apoptotic markers, i.e., cytosolic cytochrome C (cyt c), caspase-3 and caspase-9 in the pups exposed to HI, indicating neuronal cell death. However, the HI-induced increase in the expression levels of these pro-apoptotic factors was reduced by luteolin treatment.

Conclusion: These results suggest that luteolin protects postnatal rat pups from hypoxic ischemic-induced brain damage (neuronal cell death) due to its antioxidant and free radical-scavenging activities. Therefore, luteolin may be a potential neuroprotective agent in the management of HI-associated complications.

Keywords: Antioxidants, Hypoxia, Ischemia, Luteolin, Neuronal cell death, Neuroprotection