Dose-Responsive Mitigation of Hepatic Oxidative Stress and Histopathological Damage by Channa striata Extract in Post-Carbon Tetrachloride-Exposed Rats
Jul 2026· Jurnal Penelitian Pendidikan IPA· 0 citations· 40 references
TL;DR
Channa striata extract demonstrates dose-dependent ameliorative activity against established CCl₄-induced oxidative liver injury, as evidenced by attenuation of lipid peroxidation and mitigation of histopathological damage.
Abstract
Carbon tetrachloride (CCl₄) is widely used to induce experimental oxidative liver injury through the generation of free radicals that promote lipid peroxidation and hepatocellular damage. Natural products with antioxidant properties are being explored for their potential to mitigate such injury. This study aimed to evaluate the dose-responsive ameliorative effects of Channa striata extract on hepatic oxidative stress and histopathological alterations in rats following subacute CCl₄ exposure. Thirty male Wistar rats were divided into five groups: normal control (K1), CCl₄ control (K2), and three treatment groups receiving C. striata extract at 100, 150, and 200 mg/kg body weight/day for two weeks after six weeks of CCl₄ induction (K3–K5). Hepatic malondialdehyde (MDA) levels were measured as an indicator of lipid peroxidation. Liver histopathology was assessed for hepatocellular necrosis, congestion, and inflammatory cell infiltration using a semi-quantitative scoring system. CCl₄ exposure significantly increased hepatic MDA levels and caused severe histopathological damage in the control group. C. striata extract dose-dependently attenuated MDA levels (p < 0.001), with the 200 mg/kg/day group showing the lowest levels (2.80 ± 0.15 vs. 6.65 ± 0.13 nmol/g in CCl₄ control). Histopathological scores for necrosis, congestion, and inflammatory infiltration ameliorated progressively with increasing doses, with median total scores improving from 8.5 (CCl₄ control) to 2.0 (200 mg/kg/day). Channa striata extract demonstrates dose-dependent ameliorative activity against established CCl₄-induced oxidative liver injury, as evidenced by attenuation of lipid peroxidation and mitigation of histopathological damage. Further studies incorporating serum liver enzymes and molecular mechanisms are warranted.
Abstract Objectives This study aimed to investigate the interactions between biochemical, oxidative, and morphological markers of liver injury in an experimental model of alcoholic hepatitis and to evaluate the hepatoprotective efficacy of a herbal phytocomplex (AZHEPOFIT) within an integrated mechanistic framework. Methods Alcoholic hepatitis was induced in 40 male rats by oral ethanol administration combined with a high-fat diet for 21 days. From day 22, animals received AZHEPOFIT (1 mL/100 g body weight) daily for 14 days. Biochemical parameters, oxidative stress markers, antioxidant status, lipid profile, and liver histomorphology were assessed. Correlation analysis was performed using Spearman’s coefficient. Results Alcoholic hepatitis was associated with pronounced cytolysis, cholestasis, oxidative stress, dyslipidemia, and marked histopathological alterations, including steatosis, hepatocyte ballooning, inflammation, necrosis, and early fibrosis. AZHEPOFIT administration significantly reduced cytolytic enzyme activity and lipid peroxidation, enhanced antioxidant defense, improved lipid metabolism, and attenuated structural liver damage. Strong correlations exist between oxidative stress markers and cytolytic enzymes, and inverse relationships with antioxidant parameters, indicating a coordinated pathogenic network linking oxidative stress, lipid metabolism, and hepatocellular injury. Conclusions The hepatoprotective effects of AZHEPOFIT are associated with the modulation of interconnected oxidative stress–metabolic pathways. These findings provide mechanistic insight into phytotherapeutic intervention in alcohol-induced liver injury and support targeting redox-dependent pathways as a promising therapeutic strategy.
R. Jafarova, S. Guliyeva, S.A. Abasova et al.· Journal of Complementary and...· 0 citations
Liver diseases are a major global health burden, and oxidative stress plays
a key role in the development of hepatocellular injury. Mimusops elengi L. fruits contain bioactive
phytochemicals with reported antioxidant properties. This study aimed to evaluate the hepatoprotective
activity of aqueous Mimusops elengi fruit extract against carbon tetrachloride (CCl4)-induced
liver injury in Wistar rats.
Male Wistar rats were randomly allocated into five groups (n = 5). Hepatic injury was
induced using CCl4 (1 mL/kg, i.p.) for 15 days. Animals received Mimusops elengi fruit extract (200
and 400 mg/kg, orally) or silymarin (25 mg/kg). Serum ALT, AST, and catalase activity were evaluated,
followed by histopathological examination of liver tissues.
CCl4 administration significantly increased serum ALT and AST levels while reducing catalase
activity, indicating severe hepatic injury. Treatment with Mimusops elengi fruit extract significantly
reduced liver enzyme levels and improved antioxidant status in a dose-dependent manner.
Histopathological examination demonstrated preservation of hepatic architecture, reduced necrosis
and decreased inflammatory changes, particularly at 400 mg/kg.
The hepatopr tective activity observed may be attributed to the antioxidant and membrane-
stabilizing properties of flavonoids, tannins, and saponins present in Mimusops elengi fruits.
The biochemical and histopathological findings collectively support the traditional medicinal use of
this plant for liver protection and suggest its potential as a natural hepatoprotective agent.
Mimusops elengi fruit extract exhibits significant hepatoprotective effects against
CCl4-induced liver injury, likely mediated through antioxidant mechanisms. These findings support
its potential as a natural therapeutic agent, although further studies are required to elucidate its active
constituents and molecular pathways.
Nisha Chandila, Suresh Kumar, Manoj Kashyap· The International Journal of...· 0 citations
It is demonstrated that MAL induces hepatotoxicity by promoting oxidative stress, inflammation, and apoptosis, whereas morin exerts significant hepatoprotective effects, likely through modulation of antioxidant defense systems and apoptotic pathways.
Seval Yılmaz, Eda I. Demirbağ, Hakan Bağ et al.· Environmental Toxicology· 0 citations
FSN-LNPs provided enhanced hepatoprotection against DEHP-induced toxicity compared with free FSN, which was associated with attenuation of oxidative stress and inflammation and modulation of apoptosis- and ferroptosis-related pathways, likely due to improved bioavailability and cellular delivery.
Ahmed Al-Emam, Hesham M. Hassan, E. Elmorsy et al.· Naunyn-Schmiedeberg's Archiv...· 0 citations
Pretreatment with PEIV significantly mitigated effects of LPS-induced liver injury by regulating biochemical parameters, reducing oxidative stress and inflammation, and preserving liver architecture, suggesting its potential as a natural therapeutic agent for liver diseases.
S. Anadozie, A³ Maryam, Theophilus I. Ebe et al.· Comparative Clinical Patholo...· 0 citations
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