Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Octreotide ameliorates hypoxia/reoxygenation-induced cerebral infarction by inhibiting oxidative stress, inflammation and apoptosis, and via inhibition of TLR4/MyD88/NF-κB signaling pathway

Yanbin Hou¹, Zhongze Lou^1,3, Yunxin Ji¹, Liemin Ruan¹, He Gao²

¹Department of Psychosomatics, Ningbo First Hospital, Ningbo, China; ²Department of Psychiatry, Ningbo Kangning Hospital, Ningbo, China.

For correspondence:- He Gao Email: 812478044@qq.com Tel:+8615958272157

Accepted: 3 October 2021 Published: 30 November 2021

Citation: Hou Y, Lou Z, Ji Y, Ruan L, Gao H. Octreotide ameliorates hypoxia/reoxygenation-induced cerebral infarction by inhibiting oxidative stress, inflammation and apoptosis, and via inhibition of TLR4/MyD88/NF-κB signaling pathway. Trop J Pharm Res 2021; 20(11):2261-2266 doi: 10.4314/tjpr.v20i11.4

© 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 explore the effects of octreotide (OCT) on oxidative stress, inflammation and apoptosis in hypoxia/reoxygenation (H/R)-induced cerebral infarction.

Methods: The in vitro model of cerebral infarction was established by treating N2A cells with hypoxia for 4 h and reoxygenation for 24 h. The viability of N2A cells was determined by CCK-8 assay. The cells were divided into 3 groups: control group, H/R group, and H/R+OCT group. The cells in H/R+OCT group were pretreated with OCT (60 ng/mL) before H/R treatment. The oxidative stress of N2A cells were assessed by determining the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), reactive oxygen species (ROS) and malondialdehyde (MDA). Inflammation of N2A cells was evaluated by evaluating the levels of TNF-α, IL-1β, IL-6, and IL-8, while the apoptosis of N2A cells was assessed by flow cytometry. Western blot analysis was used to determine the expression of Bcl-2, Bax, TLR4, MyD88, and NF-κB.

Results: Octreotide treatment significantly reduced the level of oxidative stress. The inflammation of N2A cells caused by hypoxia/reoxygenation was inhibited by treatment with octreotide. Apoptosis of N2A cells was also inhibited by octreotide treatment. Hypoxia/reoxygenation activated TLR4/MyD88/NF-κB signaling pathway, while octreotide inhibits the activation of this pathway.

Conclusion: The results reveal that octreotide inhibits hypoxia/reoxygenation-induced oxidative stress, as well as the inflammation, and apoptosis of N2A cells by inhibiting TLR4/MyD88/NF-κB signaling pathway. Thus, these findings may provide new insights into the treatment of cerebral infarction.

Keywords: Octreotide, Cerebral infarction, Hypoxia/reoxygenation, Oxidative stress, Inflammation, Apoptosis, TLR4/MyD88/NF-?B signaling pathway