ArticleExperimental and therapeutic medicine2021
Baicalein pre-treatment alleviates hepatic ischemia/reperfusion injury in mice by regulating the Nrf2/ARE pathway.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Extract ofInternational journal of molecular sciences · 2025Article
- The Therapeutic Potential of Garlic-Derived Organic Polysulfides for Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
- Mechanism of Reactive Oxygen/Nitrogen Species in Liver Ischemia-Reperfusion Injury and Preventive Effect of Chinese Medicine.Chinese journal of integrative medicine · 2025Review
- Baicalein improves the chemoresistance of ovarian cancer through regulation of CirSLC7A6.Journal of ovarian research · 2023Article
- Chlorogenic Acid Alleviates Hepatic Ischemia-Reperfusion Injury by Inhibiting Oxidative Stress, Inflammation, and Mitochondria-Mediated Apoptosis In Vivo and In Vitro.Inflammation · 2023Article
- Nrf2-mediated therapeutic effects of dietary flavones in different diseases.Frontiers in pharmacology · 2023Review
- The Role of Pyroptosis and Autophagy in Ischemia Reperfusion Injury.Biomolecules · 2022Review
- Detoxification technology and mechanism of processing withFrontiers in pharmacology · 2022Article
- Baicalein Alleviates Testicular Ischemia-Reperfusion Injury in a Rat Model of Testicular Torsion-Detorsion.Oxidative medicine and cellular longevity · 2022Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic ischemia-reperfusion injury (HIRI) is caused by blood flow recovery following ischemia. Baicalein (BAI), a natural antioxidant used in traditional Chinese medicine, eliminates excessive free radicals and protects the structure of the cell membrane. However, its protective mechanism against HIRI is still unclear. The present study investigated underlying mechanism using a mouse HIRI model. Liver injury was evaluated using serum levels of alanine aminotransferase and aspartate aminotransferase, and hematoxylin-eosin staining was performed to evaluate the pathological changes in liver tissue. Apoptosis of hepatocytes was detected by TUNEL staining. The expression levels of reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) in the liver were detected to evaluate oxidative stress. Western blotting was performed to assess expression levels of nuclear factor E2-related factor 2 (Nrf2)/antioxidant response elements (ARE) pathway proteins in liver tissue. BAI pre-treatment significantly decreased elevation of serum aminotransferase levels induced by IR and alleviated histological damage to the liver. BAI decreased production of ROS and MDA in liver tissue induced by IR and increased the activity of SOD. At the same time, BAI inhibited apoptosis of liver cells induced by oxidative stress. Furthermore, BAI promoted the translocation of Nrf2 into the nucleus and increased the expression of total heme oxygenase-1 and NAD(P)H dehydrogenase quinone-1. The Nrf2 inhibitor ML385 reversed the protective effect of BAI on HIRI. These results indicated that BAI served a protective effect in HIRI by regulating the Nrf2/ARE pathway.
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