The therapeutic benefits of epigallocatechin gallate in rats with experimentally induced ulcerative colitis are achieved by influencing inflammation and apoptosis

表没食子儿茶素没食子酸酯对实验性溃疡性结肠炎大鼠的治疗作用是通过影响炎症和细胞凋亡实现的。

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Abstract

BACKGROUND: The potential therapeutic effects of epigallocatechin gallate (EGCG), a compound found in green tea with antioxidant and anti-inflammatory properties, on ulcerative colitis (UC) rats is a significant area of research. This study aimed to investigate the impact of EGCG on inflammation and apoptotic pathways in UC rats. METHODS: The study involved inducing UC in rats by administering 2 mL of 4% acetic acid. The UC rats were then treated with 20 mg/kg of EGCG. Colon samples were collected to evaluate gene and protein expression of various factors, including nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), tumor necrosis factor alpha (TNF-α), sphingosine kinase 1 (SphK1), macrophage inflammatory protein 1-alpha (MIP-1α), B-cell lymphoma 2 (BCL2), and BCL2 associated X (BAX), as well as the activities of caspase-3/8/9. Additionally, colon sections were stained with Masson trichrome to investigate tissue fibrosis. RESULTS: Microscopic examination of rat colonic sections stained with Masson trichrome revealed severe damage to the intestinal glands, marked by widespread hemorrhage and extensive fibrosis. Treatment with EGCG reduced the severity of the damage. Additionally, EGCG decreased the expression of several proinflammatory markers, such as NFκB and TNF-α, as well as SphK1, MIP-1α and BAX, reduced caspase-3/8/9 activity, and increased the expression of BCL2. CONCLUSIONS: The protective effects of EGCG against UC experimentally induced in rats are achieved by reducing the expression of inflammatory markers such as NFκB, TNF-α and MIP-1α, inhibiting apoptosis by decreasing the expression of BAX and caspases, and increasing the expression of BCL2.

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