4.5 Article

Erxian decoction inhibits apoptosis by activating Akt1 and repairs spinal cord injury in rats

Journal

HELIYON
Volume 8, Issue 11, Pages -

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.heliyon.2022.e11279

Keywords

Spinal cord injury; Akt1; Apoptosis

Funding

  1. National Natural Science Foun-dation of China
  2. [82174166]

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Through network pharmacology and molecular docking analysis, it was revealed that Erxian Decoction (EXD) inhibits apoptosis by activating Akt1, reducing spinal cord edema and restoring motor function in spinal cord injury (SCI) rats.
Objective: Spinal cord injury (SCI) often leads to severe physiological and pathological changes in patients. Erxian Decoction (EXD) is effective in the postoperative treatment of spinal cord injury, but its specific mechanism of action is poorly defined. Methods: Network pharmacology and molecular docking were used to predict the potential mechanisms of EXD in SCI. In vivo studies were used to validate the above predictions. For in vivo study, the rats were pretreated with or without EXD (5.76 g/kg, by intragastric gavage). Multiple molecular biological test methods to identify molecular mechanisms. One-way analysis of variance (ANOVA) was used with Bonferroni's post-hoc test to identify the differences between groups. Results: In vivo studies have shown that EXD improved motor function at 7dpi in SCI rats (P < 0.0001), signifi-cantly reduced spinal cord edema (P 1/4 0.0139), upregulated 5-HT, GFAP, and TMEM119 expression. Through network pharmacology analysis, we found that Akt1 in EXD plays a role in treating SCI. The underlying mech-anism may be the inhibition of apoptosis after activation of Akt1 phosphorylation. Molecular docking revealed that the key compounds could spontaneously bind to the Akt1 protein. Pharmacological inhibition of Akt1 activation by MK-2206, attenuated the anti-apoptotic effect of EXD on SCI in rats (P < 0.0001). Conclusions: EXD inhibits apoptosis by activating Akt1, reduce spinal cord edema and restore behavioral function after SCI in rats.

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