%0 Journal Article
%T Benificial Effect of Stachydrine on the Traumatic Brain Injury Induced Neurodegeneration by Attenuating the Expressions of Akt/mTOR/PI3K and TLR4/NF¦Ê-B Pathway
%A Nianzu Yu
%A Si Hu
%A Zheng Hao
%J Archive of "Translational Neuroscience".
%D 2018
%R 10.1515/tnsci-2018-0026
%X Present investigation aims to explore the protective effect of stachydrine against traumatic brain injury (TBI) and also investigate the molecular mechanism of its action. TBI was induced by the fall a hammer (450 g) from the height of 1.5 m. and later stachydrine was administered for 2 weeks starting 2 hr after the induction of TBI. Effect of stachydrine was determined by estimating modified neurological severity score (mNSS), percentage of water content in the brain and cognitive dysfunction in TBI rats. Moreover western blot assay, histopathology and enzyme linked immunosorbent assay (ELISA) tests were used to determine the effect of stachydrine on TBI injured rats. Result of the report suggests that stachydrine reduces the mNSS and percentage of water content in the brain and also attenuates the cognitive dysfunction in TBI injured rats. However data of western blot assay reports that stachydrine reduces the expression of PI3K/m-TOR/Akt pathway in the brain tissues of TBI rats. Concentration of interleukin (IL-1¦Â), tumor necrosis factor-¦Á (TNF-¦Á) and interferon gamma (INF-¦Ã) was reduces in stachydrine treated group than TBI group. Moreover expression of Nuclear factor-¦ÊB/Toll-like receptor 4 (NF-¦ÊB/TLR-4) protein was also decreased in stachydrine treated group than TBI group. Histopathology study on brain tissue reveals that the percentage of apoptotic cells was also reduced in stachydrine treated group than TBI group. Data of this investigation concludes that stachydrine protects the neuronal injury by attenuating the phosphatidylinositide 3-kinases/mammalian target of rapamycin/Protein kinase B (PI3K/m-TOR/Akt) and NF-¦ÊB/TLR-4 pathway in TBI injured rats
%K Stachydrine
%K Traumatic brain injury
%K Apoptosis
%K Inflammation
%K TLR-4
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6341910/