Publications by authors named "Xiaodie Sun"
The prevalence and mortality rates of colorectal cancer have been increasing in recent years, driven in part by the reliance of cancerous cells on aerobic glycolysis for growth. Sodium butyrate (NaB) has been shown to impede this process in colorectal cancer cells, although its mechanism of action remains unclear. In this study, we used cobalt chloride (CoCl) to simulate a hypoxic environment and demonstrated that NaB downregulated hypoxia-inducible factor-1α (HIF-1α) protein levels under both normoxic and hypoxic conditions.
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- Sodium butyrate (NaB), a short-chain fatty acid from dietary fiber fermentation, is explored for its effects on ulcerative colitis (UC) and its mechanisms of action against inflammation and oxidative stress.
- In a murine colitis model induced by DSS, NaB improved various metrics of colitis severity, reduced oxidative stress markers, and activated important signaling pathways involved in inflammation regulation.
- The study concludes that NaB mitigates UC symptoms by suppressing oxidative stress and inflammatory responses through pathways like COX-2/Nrf2/HO-1 and promoting mitophagy, indicating its potential as a therapeutic agent for UC.
Article Synopsis
- Colorectal cancer (CRC) is a common and serious health issue, and while sodium butyrate (NaB), a byproduct of fiber fermentation, has shown promise in inhibiting CRC, its mechanism of action remains unclear.
- In laboratory studies, NaB was found to induce ferroptosis (a type of cell death) and apoptosis (programmed cell death) in colorectal tumor cells (HCT-116) but had limited effects on normal intestinal cells (FHC).
- Results indicated that NaB increases iron levels and depletes glutathione in CRC cells, with CD44 and SLC7A11 identified as key signaling molecules involved in NaB's mechanism, especially when combined with ferroptosis