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Effect of Ranae Oviductus Protein Hydrolysate on Ethanol-induced L-02 Cell Injury / 中国实验方剂学杂志
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 43-50, 2021.
Article Dans Chinois | WPRIM | ID: wpr-906361
ABSTRACT

Objective:

To study the protective effect and mechanism of Ranae Oviductus protein hydrolysate (ROPH) on the expression of pathway-related proteins in ethanol-induced L-02 cell injury.

Method:

The ROPH was prepared by compound enzymatic hydrolysis. L-02 cell injury model was induced with 400 mmol·L<sup>-1 </sup>ethanol. Cell viability was detected by cell counting kit-8 (CCK-8) assay. Cell cycle and apoptosis were examined by flow cytometry. JC-1/Hochest staining was employed for qualitative investigation. The expression of related proteins in apoptosismitogen-activated protein kinase (MAPK) signaling pathway, and pyroptosis in L-02 cells was detected by Western blot.

Result:

The results of the CCK-8 assay showed that 400 mmol·L<sup>-1 </sup>ethanol could induce L-02 cell injury within 12 hours. Compared with the blank group, the model group showed decreased viability of L-02 cells (<italic>P</italic><0.01), elevated percentage of the cell cycle in the G<sub>0</sub>/G<sub>1</sub> phase (<italic>P</italic><0.01), increased total cell apoptosis rate (<italic>P</italic><0.01), reduced mitochondrial membrane potential (<italic>P</italic><0.01), up-regulated expression of apoptosis-related proteinsB-cell lymphoma-2 (Bcl-2)-associated X protein (Bax), Cytochrome C (Cyt C), and cysteine-dependent aspartate specific protease-3 (Caspase-3)] (<italic>P</italic><0.05, <italic>P</italic><0.01) and MAPK signaling pathway-related proteinsC-Jun amino-terminal kinase (JNK) and p38 MAPK] (<italic>P</italic><0.05, <italic>P</italic><0.01), and potentiated expression of pyrolysis-related proteins Caspase-1 and interleukin-1<italic>β </italic>(IL-1<italic>β</italic>) (<italic>P</italic><0.05). Compared with the model group, the ROPH treatment group exhibited improved cell cycle arrest (<italic>P</italic><0.05, <italic>P</italic><0.01), diminished total cell apoptosis rate (<italic>P</italic><0.01), elevated mitochondrial membrane potential in a dose-dependent manner, down-regulated expression of Bax, Cyt C, and Caspase-3 proteins (<italic>P</italic><0.05, <italic>P</italic><0.01), up-regulated expression of Bcl-2 protein (<italic>P</italic><0.05, <italic>P</italic><0.01), and a downward trend in expression of proteins related to MAPK signaling pathway and pyrolysis (<italic>P</italic><0.05, <italic>P</italic><0.01).

Conclusion:

ROPH could inhibit oxidative stress-triggered liver injury in ethanol-induced cells by improving mitochondrial membrane potential, reducing the expression of proteins in the mitochondria-mediated apoptosis pathway, and inhibiting the expression of proteins related to the MAPK signaling pathway and pyrolysis pathway to reduce the mitochondrial dysfunction and inflammatory response in ethanol-induced L-02 liver cells and inhibit oxidative stress, thereby exerting a therapeutic role in alcoholic liver injury.

Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) Type d'étude: Recherche qualitative langue: Chinois Texte intégral: Chinese Journal of Experimental Traditional Medical Formulae Année: 2021 Type: Article

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Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) Type d'étude: Recherche qualitative langue: Chinois Texte intégral: Chinese Journal of Experimental Traditional Medical Formulae Année: 2021 Type: Article