Research Paper Volume 13, Issue 8 pp 11207—11217
Panax notoginseng protects the rat brain function from traumatic brain injury by inhibiting autophagy via mammalian targeting of rapamycin
- 1 Department of Intensive Care Unit, The First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, China
- 2 Zhejiang Chinese Medical University, Hangzhou, China
- 3 Department of Pharmacology of College of Medicine and Health, Lishui University, Lishui, China
- 4 Department of Pharmacology, Zhejiang University School of Medicine, Hangzhou, China
- 5 Department of Intensive Care Unit, The First Affiliated Rehabilitation Hospital of Zhejiang Chinese Medical University, The First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, China
Received: August 31, 2020 Accepted: February 16, 2021 Published: April 4, 2021https://doi.org/10.18632/aging.202790
How to Cite
Copyright: © 2021 Shi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Traumatic brain injury (TBI) remains one of the leading causes of death and disability worldwide. Our previous studies have found that traditional Chinese medicine, Panax notoginseng (P. notoginseng) 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), P. notoginseng group (experimental group), Rapamycin group, and Panax notoginseng+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), Beclin 1, 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, Beclin 1, 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, Beclin 1, 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 the P. notoginseng group (M+PN group, the group showing signs of TBI with P. notoginseng treatment). Also, there was no significant difference between P. notoginseng group and P. notoginseng+Rapamycin group (M+PN+Rapa group, the group showing signs of TBI with P. notoginseng+Rapamycin treatment). P. notoginseng protects the rat brain function from TBI by inhibiting autophagy through the mTOR signaling pathway and other autophagy pathways.
TBI: Traumatic brain injury; mTOR: mammalian target of rapamycin; P62: sequestosome 1; LC3: microtubule-associated protein 1 light chain 3; TEM: transmission electron microscope; P. notoginseng: Panax notoginseng.