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Shuganning Injection Suppresses Apoptosis for Protecting Against Cantharidin-Induced Liver Injury by Network Pharmacology and Experiment Validation.
Duan, Xiaotong; Ao, Jingwen; Yu, Ming; Li, Sali; Li, Xiaofei; Zhang, Jianyong.
Afiliación
  • Duan X; School of Basic Medicine, Zunyi Medical University, Zunyi, Guizhou 563000, China.
  • Ao J; School of Pharmacy, Zunyi medical university, Zunyi, Guizhou 563000, China.
  • Yu M; School of Pharmacy, Zunyi medical university, Zunyi, Guizhou 563000, China.
  • Li S; School of Basic Medicine, Zunyi Medical University, Zunyi, Guizhou 563000, China.
  • Li X; School of Basic Medicine, Zunyi Medical University, Zunyi, Guizhou 563000, China.
  • Zhang J; School of Pharmacy, Zunyi medical university, Zunyi, Guizhou 563000, China.
ACS Omega ; 9(12): 13692-13703, 2024 Mar 26.
Article en En | MEDLINE | ID: mdl-38559921
ABSTRACT
Cantharidin (CTD) is a compound of mylabris with antitumor activity, and CTD can potentially cause toxicity, especially hepatotoxicity. The classical Traditional Chinese Medicine prescription Shuganning injection (SGNI) exerts notable anti-inflammatory and hepatoprotective effects. However, the protective property and mechanism of SGNI against CTD-induced liver injury (CTD-DILI) have not yet been elucidated. To investigate the effective compounds, potential targets, and molecular mechanism of SGNI against CTD-DILI, network pharmacology combined with experiments were performed. This study found that SGNI could act with 62 core therapeutic targets, regulate multiple biological processes such as apoptosis, and oxidative stress, and influence apoptotic and p53 signaling pathways to treat CTD-DILI. Subsequently, HepaRG cell experiments demonstrated that SGNI pretreatment significantly increased the levels of GSH-Px and SOD, inhibiting the apoptosis induced by CTD. In vivo, according to H&E staining, SGNI can reduce the degeneration of hepatocytes and cytoplasmic vacuolation in mice exposed to CTD. Western blot analysis results indicated that SGNI pretreatment significantly suppressed the expressions of Caspase-3 and Bax while increasing the expression of Bcl-2. In conclusion, SGNI acted as a protective agent against CTD-DILI by inhibiting apoptosis.

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: ACS Omega Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: ACS Omega Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos