ArticleMolecular and cellular biochemistry2013
Hepatoprotective potential of new steroid against carbon tetrachloride-induced hepatic injury.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 12 citations in OpenAlex.
- Therapeutic Role of Probiotics Against Environmental-Induced Hepatotoxicity: Mechanisms, Clinical Perspectives, Limitations, and Future.Probiotics and antimicrobial proteins · 2025Review
- Vitamin B combination reduces fluconazole toxicity in Wistar rats.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2019Article
- Preliminary evaluation of hepatoprotective potential of the polyherbal formulation.Journal of intercultural ethnopharmacologyArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was designed to evaluate the hepatoprotective effects of newly isolated stigmast-4, 20 (21), 23-trien-3-one (STO) against carbon tetrachloride-induced hepatic injury in Wistar albino rats. Hepatotoxicity was induced by the administration of a single intraperitoneal dose of CCl4 (0.5 mL/kg CCl4 in olive oil) in experimental rats. Three different doses (2.5, 5.0, and 10 mg/kg, p.o) of STO was administered to the test groups during whole experimental protocol. Changes in the activity of serum ALT, AST, ALP, TB, and TP, anti-oxidant enzymes like SOD, CAT, GPx, GST, and LPO were studied in CCl4-induced hepatocellular carcinogenesis. The altered levels of serum ALT, AST, ALP, TB, and TP restored toward normalization significantly by STO in a dose dependant manner. The biochemical observations were supplemented with histopathological examination of rat liver sections. Meanwhile, it also produced a significant and dose-dependent reversal of CCl4-diminished activity of anti-oxidant enzymes like SOD, CAT, GPx, GST, and the reduced CCl4-elevated level of LPO. STO significantly prevented the increased levels of serum markers, also suppressed the free radical processes by scavenging hydroxyl radicals. It also modulates the levels of LPO and markedly increases the endogenous anti-oxidant enzymes level in CCl4-induced hepatic injury.
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