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Study on the Role of Schisandrin B in Ameliorating Hepatic Ischemia-Reperfusion Injury by Modulating Hepatocyte Autophagy
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Background: Hepatic ischemia-reperfusion injury (HIRI) significantly affects the prognosis of liver surgery, such as hepatocellular carcinoma resection and liver transplantation. However, the pathogenesis of HIRI has not been fully elucidated, and prevention and treatment strategies remain challenging. Methods: A mouse model of HIRI was established, and schisandrin B (Sch B) was used to intervene in HIRI. The effect of Sch B on HIRI was assessed using hematoxylin and eosin (HE) staining, quantitative polymerase chain reaction (qPCR), Western blot (WB), immunohistochemistry, and enzyme-linked immunosorbent assay (ELISA). Results: The expression of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the serum of the HIRI mouse model was significantly increased, indicating the successful construction of the HIRI mouse model. In the Sch B intervention group, serum ALT and AST levels were significantly decreased. Hematoxylin and eosin staining and qPCR results demonstrated that Sch B could reduce HIRI in mice. The qPCR and immunohistochemistry showed that Sch B reduced HIRI in mice by decreasing the expression of autophagy-related factors Beclin-1 and LC3-II. Conclusions: Additionally, qPCR and immunohistochemical results indicated that Sch B reduced HIRI by decreasing the expression of autophagy-related factors (Beclin-1 and LC3-II) and hepatocyte damage-related factors (caspase-3, caspase-9, and Bax), thereby reducing HIRI in mice. The results of electron microscopy, immunohistochemistry, and qPCR confirmed that Sch B could reduce autophagy and alleviate HIRI.
Title: Study on the Role of Schisandrin B in Ameliorating Hepatic Ischemia-Reperfusion Injury by Modulating Hepatocyte Autophagy
Description:
Background: Hepatic ischemia-reperfusion injury (HIRI) significantly affects the prognosis of liver surgery, such as hepatocellular carcinoma resection and liver transplantation.
However, the pathogenesis of HIRI has not been fully elucidated, and prevention and treatment strategies remain challenging.
Methods: A mouse model of HIRI was established, and schisandrin B (Sch B) was used to intervene in HIRI.
The effect of Sch B on HIRI was assessed using hematoxylin and eosin (HE) staining, quantitative polymerase chain reaction (qPCR), Western blot (WB), immunohistochemistry, and enzyme-linked immunosorbent assay (ELISA).
Results: The expression of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the serum of the HIRI mouse model was significantly increased, indicating the successful construction of the HIRI mouse model.
In the Sch B intervention group, serum ALT and AST levels were significantly decreased.
Hematoxylin and eosin staining and qPCR results demonstrated that Sch B could reduce HIRI in mice.
The qPCR and immunohistochemistry showed that Sch B reduced HIRI in mice by decreasing the expression of autophagy-related factors Beclin-1 and LC3-II.
Conclusions: Additionally, qPCR and immunohistochemical results indicated that Sch B reduced HIRI by decreasing the expression of autophagy-related factors (Beclin-1 and LC3-II) and hepatocyte damage-related factors (caspase-3, caspase-9, and Bax), thereby reducing HIRI in mice.
The results of electron microscopy, immunohistochemistry, and qPCR confirmed that Sch B could reduce autophagy and alleviate HIRI.
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