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Abstract Title:

protects the rat brain function from traumatic brain injury by inhibiting autophagy via mammalian targeting of rapamycin.

Abstract Source:

Aging (Albany NY). 2021 Apr 4 ;13. Epub 2021 Apr 4. PMID: 33819197

Abstract Author(s):

Ying Shi, Xiaqing Zhou, Ruhui Yang, Songmin Ying, Lingcong Wang

Article Affiliation:

Ying Shi

Abstract:

Traumatic brain injury (TBI) remains one of the leading causes of death and disability worldwide. Our previous studies have found that traditional Chinese medicine,() can reduce cerebral hemorrhage in rats with TBI. Yet, the exact mechanism still remains unclear. According to the random number table, 36 SD rats were randomly divided into six groups: Sham group (negative control group), Model group, PIK inhibitor group (positive group),group (experimental group), Rapamycin group, and+Rapamycin group (experimental group). In the Model group (M group, the group showing signs of TBI without any treatment), the neural function defect score was significantly decreased, while sequestosome 1 (P62), Becline1, and microtubule-associated protein 1 light chain 3 (LC3-II) were significantly increased. The brain tissue was significantly damaged, and many autophagosomes were observed in the cytoplasm. Compared with the Model group and the Rapamycin group (M+Rapa group, the group showing signs of TBI with Rapamycin treatment), P62, Becline1, and LC3-II were significantly decreased, the score of neural function defect was significantly improved, and the brain tissue damage was significantly reduced in the PIK (phosphatidylinositol 3-kinase) inhibitor group (M+LY group, the group showing signs of TBI with PIK inhibitor treatment). Compared with the Model group, mTOR was decreased and LC3-II was increased; however, there were no significant changes in neural function defect score, HE staining, Nissl staining, and transmission electron microscopy in the Rapamycin group. Compared with the Model group, the neural function defect score at 72h was significantly improved, mTOR was significantly increased, P62, Becline1, and LC3-II significantly decreased, brain tissue damage was reduced in HE staining and Nissl staining, autophagosomes were reduced in cytoplasm by transmission electron microscopy in thegroup (M+PN group, the group showing signs of TBI withtreatment). Also, there was no significant difference betweengroup and+Rapamycin group (M+PN+Rapa group, the group showing signs of TBI with+Rapamycin treatment).protects the rat brain function from TBI by inhibiting autophagy through the mTOR signaling pathway and other autophagy pathways.

Study Type : Animal Study

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