AI Article Synopsis
- This study investigated how Gandankang (GDK) aqueous extract helps reduce acute liver injury caused by carbon tetrachloride (CCl) in both mice and liver cells (HepG2).
- The results indicate that GDK not only prevents liver damage but also improves liver function by blocking inflammatory and oxidative stress pathways.
- GDK appears to work by inhibiting liver fibrosis, regulating proteins related to oxidative stress, and reducing lipid peroxide generation, thereby protecting liver cells from damage.
Article Abstract
The aims of this study were to evaluated the effect and underlying mechanism of Gandankang (GDK) aqueous extract in alleviating the acute liver injury induced by carbon tetrachloride (CCl) in vivo and in vitro. Mice were divided into 5 groups (n = 8) for acute (Groups: control, 0.3 % CCl, BD (Bifendate), 1.17, 2.34 and 4.68 mg/kg GDK) liver injury study. 10 µL/g CCl with corn oil were injected interperitoneally (i.p) expect the control group. HepG2 cells were used in vitro study. The results showed GDK can effectively inhibit liver damage and restore the structure and function of the liver. In mechanism, GDK inhibited CCl-induced liver fibrosis and blocked the NF-κB pathway to effectively inhibit the hepatic inflammatory response; and inhibited CCl-induced oxidative stress by upregulating the Keap1/Nrf2 pathway-related proteins and promoting the synthesis of several antioxidants. Additionally, it inhibited ferroptosis in the liver by regulating the expression of ACSl4 and GPX4. GDK reduced lipid peroxide generation in vitro by downregulating the production of reactive oxygen species and Fe aggregation, thereby inhibiting ferroptosis and alleviating CCl-induced hepatocyte injury. In conclusion, we describe the potential complex mechanism underlying the effect of GDK against acute liver injury.
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| http://dx.doi.org/10.1016/j.ecoenv.2023.114527 | DOI Listing |
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