Article · Volume 22, Issue 4 · pp. 1402–1412
Tanshinone Improves Endoplasmic Reticulum Stress Injury in Mice with Ischemic Cerebral Infarction by Regulating miR-29 and Inhibiting PI3K/Akt Signaling Pathway
Bo Xiong1, Jianju Zhou2, Hang Li1, Yuanchao Wen1
- 1Department of Neurosurgical Center—Cerebrovascular Disease, Zunyi First People’s Hospital, Zunyi, Guizhou, China.
- 2Department of Neurological Rehabilitation, Zunyi First People’s Hospital, Zunyi, Guizhou, China.
Abstract
Background: Tanshinone (TSL) is a good traditional Chinese medicine with a wide range of applications. Whether it plays a role in ischemic cerebral infarction is unclear. Objectives: This study aims to explore the mechanism of tanshinone (TSL) to improve endoplasmic reticulum stress injury in mice with ischemic cerebral infarction by regulating miR-29 and inhibiting the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Materials and Methods: Ischemic cerebral infarction mouse models were constructed and divided into the NC group, TSL group, TSL+miR-29mimic group, and TSL+miR-29inhibitor group. The expression of P-EIF-2α and P-PERK in the ischemic penumbra cortical area of cerebral infarction lesions was monitored, brain cell apoptosis was observed, and genes related to the miR-29 and PI3K/Akt pathways in the tissue were detected. Results: A cerebral infarction model was successfully prepared. Compared with the sham operation group, the cerebral infarction site was severely ischemic and larger; TSL had an improved effect on ischemic cerebral infarction, and polydopamine-based nanoparticles (PDA NPs)-TSL had the best effect; TSL can reduce the expression of P-PERK in the cortical area and inhibit the expression of P-EIF-2α in the cortical area of the ischemic penumbra, and TSL has a more significant effect in this aspect. By using agonists and inhibitors of miR-29, TSL promotes the expression of miR-29 and improves endoplasmic reticulum stress injury in mice with ischemic cerebral infarction by inhibiting the PI3K/Akt signaling pathway. Conclusion: TSL has a good anti-inflammatory effect, can reduce the expression of P-PERK in the cortical area, inhibit the expression of P-EIF-2α in the ischemic penumbra cortical area, and inhibit PI3K/Akt signaling by promoting miR-29 pathway to improve endoplasmic reticulum stress damage in mice with ischemic cerebral infarction.
Keywords: Polydopamine nanoparticles; tanshinone; miR-29; PI3K/Akt; ischemic cerebral infarction; endoplasmic reticulum stress; injury
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