Neuroprotective effect of triptolide on neuronal inflammation in rats with mild brain injury

  • IBRO Neurosci Rep. 2024 May 23:17:13-21. doi: 10.1016/j.ibneur.2024.05.007.
Zhanglu Fang  1 Guanghong Shen  2 Chengjian Lou  3 Benson O A Botchway  4 Qinglin Lu  1 Qining Yang  1 Nashwa Amin  5  6
Affiliations
  • 1. Department of Orthopaedics, Jinhua Municipal Central Hospital, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, China.
  • 2. Jinhua Maternal and Child Health Hospital, Zhejiang University School of Medicine, Jinhua, China.
  • 3. Department of Neurosurgery, Fourth Affiliated Hospital, Zhejiang University School of Medicine, Yiwu 322022, China.
  • 4. Institute of Systemic Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China.
  • 5. The Affiliated People's Hospital of Hangzhou Medical College, Hangzhou Medical College, Hangzhou, China.
  • 6. Department of Zoology, Faculty of Science, Aswan University, Egypt.
Abstract

Concussions sustained while playing sports are a prominent cause of mild traumatic brain injury (mTBI), which is prevalent among teenagers. The early and intermediate stages of mild traumatic brain injury (mTBI) can be characterized by inflammation, neurodegeneration, and brain tissue edema, which can lead to permanent brain damage. The present study investigated the therapeutic effects of triptolide in mTBI and brain damage recovery. After building mTBI model in male rat, triptolide administrated daily for 1 week in the treated group. On day 3 and day 7 of administration, hippocampus tissues were collected to evaluate inflammation and Autophagy in the brain. The expressions of inflammatory factors interleukin (IL)-1β and tumor necrosis factor-alpha in serum were downregulated, while IL-10 expression was upregulated when compared with the mTBI group on day 3 and day 7. The expression of IL-10 on day 7 was higher than on day 3. Quantitative polymerase chain reaction (qPCR) analysis of inflammatory-related factors (i.e., Il-1β and nuclear factor-κB (NF-κB), and western blot as well as immunofluorescence staining of autophagy-related proteins (i.e., LC3B) and Aquaporin (AQP 4) showed lower expression on day 3 and day 7 in the triptolide-treated group. Moreover, NeuN immunostaining, and hematoxylin and eosin (HE) staining for hippocampus region revealed that the triptolide-treated group showed a decrease in damaged cells. Our findings emphasize the effectiveness of triptolide therapy after mild traumatic brain injury via modulating Autophagy, attenuating inflammation and reduces edema by decreasing AQP 4 expression.

Keywords
Autophagy; Mild traumatic brain injury; Neuro-inflammation; Triptolide.
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