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Published on: December 9, 2018
Apigenin Protects Against Ischemic Stroke Through Anti- Inflammatory Mechanisms: A Study Combining Comprehensive
Jinwen Yao1, Xu Wang2,3, Dexi Zhao2,3
1Jilin Cancer Hospital, Pharmacy Department, Changchun, Jilin, 130000, China.
Background And Objective:
There is a well-established link between inflammation and Ischemic Stroke (IS) pathology. A natural compound, Apigenin (APG), has a neuroprotective effect. However, the specific mechanisms underlying the anti-inflammatory effects of APG and its protective effects on the blood-brain barrier following IS are unclear. This study aimed to explore the mechanisms behind the anti-inflammatory effect of APG in IS.
Methods:
Male Sprague-Dawley rats were used to establish a model of unilateral middle cerebral artery occlusion (MCAO) and were administered APG by oral gavage at doses of 30, 60, or 120 mg/kg for 7 days. On the following day, brain tissues were collected after MCAO. Brain injury was evaluated by measuring brain water content, hematoxylin and eosin (H&E) staining, and Evans blue extravasation. To investigate potential proteins associated with inflammation, methods such as molecular docking, molecular dynamics simulations, Mendelian randomization analysis, immunohistochemistry, and Western blotting were employed.
Results:
APG therapy has improved neurological deficiencies, lowered brain edema, and improved blood-brain barrier integrity. It has also resulted in decreased levels of inflammatory proteins TLR4, MyD88, NFκB, IL1β, MMP9, and iNOS after IS. Furthermore, IL1R2 was identified as a potential predictive target for IS.
Discussion:
APG can repair nerve damage post-IS, with its protective effects mediated by anti-inflammatory mechanisms. The TLR4/myD88/NF-kB signaling pathway is a protective pathway of the body. APG may exert a protective effect on the blood-brain barrier after IS through the TLR4/MyD88/NF-kB signaling pathway.
Conclusion:
APG can protect against IS by inhibiting the inflammatory response, providing a theoretical basis for clinical translation and further experimental research of APG.

