ArticleAnnals of gastroenterology
The therapeutic benefits of epigallocatechin gallate in rats with experimentally induced ulcerative colitis are achieved by influencing inflammation and apoptosis.
Article in Annals of gastroenterology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.