Tanshinone Improves Endoplasmic Reticulum Stress Injury in Mice with Ischemic Cerebral Infarction by Regulating miR-29 and Inhibiting PI3K/Akt Signaling Pathway

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. Purpose 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.