CCl4-induced Hepatotoxicity Research Articles (Page 1)

Background/Objectives: The search for new bioactive molecules increasingly extends beyond conventional medicinal plants, highlighting the importance of exploring alternative botanical sources. Parasitic plants represent a promising but underexploited reservoir of pharmacologically relevant compounds. Cuscuta australis (CA), a parasitic species with a history of traditional use, remains poorly characterized. This study aimed to investigate its phytochemical composition and evaluate its antioxidant, anti-inflammatory, and hepatoprotective properties. Methods: The phytochemical profile of CA extract was characterized by LC-MS. Antioxidant capacity was assessed using DPPH and ABTS assays. In vivo hepatoprotection was evaluated in male rats subjected to CCl4-induced hepatotoxicity and treated orally with CA (30 or 60 mg/kg body weight). Biochemical, lipid, oxidative stress, and histological parameters were determined. Molecular docking was conducted to predict the binding of major identified compounds against selected protein targets. Results: CA significantly and dose-dependently improved biochemical and histological markers. At 60 mg/kg, ALT, AST, ALP, and bilirubin were reduced by 32%, 33%, 63%, and 51%, respectively. Lipid metabolism was improved by decreased TC, TG, and LDL-C with increased HDL-C. Antioxidant defense was enhanced through elevated CAT, SOD, and GPx activities, accompanied by reduced MDA levels. TNF-α and IL-6 decreased by 48% and 53%, respectively. Histopathology confirmed hepatoprotection and reduced fibrosis. Docking studies revealed strong binding affinities (−7.07 to −19.20 kcal/mol) for several metabolites, notably quercetin glucoside, diosmetin glucoside, caffeic acid glucoside, feruloylquinic acid, and isorhamnetin glucoside, against CYP450, IL-2, TNF-α, and IL-6. Conclusions: These findings demonstrate that C. australis is a promising source of bioactive compounds with hepatoprotective, antioxidant, antihyperlipidemic, and anti-inflammatory effects, supporting its potential as a natural therapeutic agent.

Mussaenda erythrophylla, a botanical treasure, has revealed numerous pharmacological potentials warranting scientific investigation. The hydroalcoholic extract of its leaves demonstrated dose-dependent analgesic, anti-inflammatory, and antipyretic activities. Notably, the leaf extract exhibited robust antioxidant activity, comparable to vitamin C, as evidenced by DPPH and NO assays. Methanolic extracts of the plant showed promising in vitro anthelmintic activity against earthworms. Additionally, root extracts in chloroform and ethanol significantly increased urine volume. Methanolic and ethyl acetate extracts of the plant protected against CCl4-induced hepatotoxicity in rats, as indicated by decreased serum enzyme levels. The plant extracts also demonstrated anti-arthritic properties through proteinase inhibition and denaturation assays. Ethanolic leaf extract showed potent anti-plasmodial activity against P. falciparum, with minimal toxicity. Furthermore, the leaf extract effectively inhibited carbon steel corrosion in a 1M HCl solution. Phytochemical analysis of floral extracts revealed the presence of steroids and triterpenoids. Keywords: Herbal remedy, Analgesic, antioxidant, Anti-arthritic, Anti-plasmodial, Corrosion inhibition

The plant Euphorbia milii (E. milii) is used as a folk medicine for the treatment of hepatitis, warts and cancer. However, the anti-oxidant and hepatoprotective activities of E.milii remain largely unknown. The present study is aimed to evaluate the anti-oxidant and hepatoprotective potential of E.milii by using various in vitro and in vivo models. Initially, two crude extracts, hydro-alcoholic and methanolic, were prepared using sonication method. The anti-oxidant assays were performed to find out the most potent crude extract, which was fractionated into five sub-fractions including n-hexane, chloroform, ethyl acetate, n-butanol and water. To investigate the most potent fraction, the anti-oxidant assays were employed. Among these fractions, ethyl acetate fraction (EMEtOAc) showed the most potent anti-oxidant effects. To prove the in vivo relevance a CCl4-induced hepatotoxicity model was employed. EMEtOAc fraction significantly inhibited the increased-level of enzymes (AST, ALT and ALP) and bilirubin in serum, and reversed the CCl4-induced lipid peroxidation and nitric oxide levels in liver tissues. Further, protective effect of EMEtOAc fraction was demonstrated by preventing the CCl4-induced histopathological changes in liver tissues. Our study suggests that EMEtOAc fraction has the potent anti-oxidant and hepatoprotective effects, and may be a promising treatment against a variety of hepatic disorders.

Liver disease is becoming the most common cause of death all over the world. Each year 5.9 % of global death is associating with alcohol-related liver disease (ALD), The current study focuses on readily available natural resources. S.amaranthoides and P. foetida plants hydroethanolic extracts demonstrated a significant hepatoprotective potential on CCl4-induced hepatotoxic Wistar rats, Alteration of serum SGOT, SGPT and Alkaline Phosphatase concentration caused by CCl4 administration was recovered by using combined plant extracts. Treatment with 500mg/kg of both plants' hydroethanolic extracts, Sphaeranthus amaranthoides and Paerida foetida, resulted in a significant decrease in the levels of ALT, AST, ALP, total protein, total bilirubin, as well as a significant increase in the levels of MDA and GSH when compared to the disease control group. When compared to the standard group given silymarin at a dose of 10mg/kg body weight, histopathological studies revealed a good hepatoprotective effect. Combined plant extracts have shown a potential impact, may be due to presence of flavonoids and phenolic content. As both plants are edible, they are safe and effective.

BACKGROUND: Prolonged exposure to constant light suppresses melatonin synthesis by the pineal gland and induces desynchronosis, increasing the risk of various pathological conditions, including liver dysfunction. Exogenous melatonin is known to exert a pronounced hepatoprotective effect; however, its role in protecting the liver against carbon tetrachloride (CCl4)-induced toxicity remains insufficiently understood. Moreover, the impact of disrupted circadian rhythmicity under melatonin deficiency on the development of liver pathology, as well as the mechanisms of melatonin’s hepatoprotective action in toxic injury. AIM: The work aimed to investigate the effects of dark deprivation and exogenous melatonin on the ultrastructure of mitochondria in rat hepatocytes under carbon tetrachloride-induced toxic liver injury. METHODS: The study involved male Wistar rats (n = 200), aged 6 months, with a body weight of (350 ± 15) g. The animals were divided into five groups: group 1, control group, fixed light–dark cycle; group 2, dark deprivation; group 3, fixed light–dark cycle with intraperitoneal CCl4 (in olive oil, 0.3 mg/kg) every 3 days; group 4, dark deprivation with CCl4 every 3 days; group 5, dark deprivation with CCl4 injections every 3 days, (intraperitoneally) and daily melatonin administration (Sigma-Aldrich, USA; intragastrically, 0.3 mg/kg). The experiment lasted 3 weeks. The ultrastructure of hepatocytes was evaluated using transmission electron microscopy. The micromorphometric analysis of mitochondria included measurement of organelle area, quantification and length of cristae, and calculation of the concentration of inner mitochondrial membranes. The statistical analysis was performed using GraphPad Prism v8.41 (GraphPad Software, USA). RESULTS: Dark deprivation caused marked structural changes in hepatocytes, including cytoplasmic swelling, nuclear deformation, ribosomal detachment from the endoplasmic reticulum, reduced mitochondrial number, shortened cristae, and decreased concentration of inner mitochondrial membranes. CCl₄ exposure resulted in more severe damage to hepatocytes, such as cytoplasmic vacuolization, mitochondrial swelling, and necrosis. Under dark deprivation, CCl₄ toxicity was exacerbated: total mitochondrial count decreased with compensatory enlargement, cristae were shortened, and the concentration of inner mitochondrial membranes declined, indicating reduced mitochondrial function. Melatonin has a protective effect, preserving nuclear morphology, reducing lipid vacuole accumulation, and normalizing micromorphometric parameters of mitochondria. CONCLUSION: Pineal melatonin deficiency under dark deprivation aggravates CCl₄-induced hepatotoxicity due to induction of oxidative stress and mitochondrial dysfunction. Melatonin demonstrates a pronounced hepatoprotective effect by stabilizing hepatocyte ultrastructure and supporting energy metabolism. These findings support the use of melatonin in preventing liver damage under chronic intoxication and circadian rhythmicity disruption.

Some conventional drugs are swiftly accessible and poorly soluble in the body. Although it is less soluble and accessible, silymarin, a well-known antioxidant drug, is used to treat several ailments. It is integrated into green-designed Fagonia cretica extract (FCE) based on PEGylated-Sily@ZnFe2O4 in this work to enhance these characteristics. UV–visible spectrometry, X-ray diffraction (XRD), scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FTIR), and zeta potential analysis were all used to thoroughly analyze the nanocomposites. As a result, ZnFe2O4 nanocomposites (NCs) produced nanostructures with an average crystal size of 7.66 nm, whereas PEGylated-Sily@ZnFe2O4 nanodrug produced with an average crystal size of 25.38 nm. The ZnFe2O4 NCs produced nanostructures with an average grain size of 332 nm and 504 nm, respectively as deduce by SEM analysis. Silymarin was estimated to have a loading efficiency of 27.39% into ZnFe2O4 NCs. To examine the produced nano-drug’s in vivo antioxidative capacity in the liver in comparison to pure silymarin, albino rats intoxicated with CCl4 were administered different dosages of 500 and 1500 μg/kg body weight. In hepatic tissue, CCl4 increased ROS and TBARS and lowered SOD, POD, and CAT levels, causing DNA damage that was mitigated subsequently by PEGylated-Sily@ZnFe2O4. In a rat model of CCl4-induced hepatotoxicity, the in vivo assessment experiments showed that the synthesized PEGylated-Sily@ZnFe2O4 efficiently displayed a hepatoprotective effect by mitigating cellular abnormalities caused by CCl4 toxication. Additionally, the PEGylated-Sily@ZnFe2O4 was shown to reduce the degree of DNA damage in the COMET experiment. In contrast to the traditional drug silymarin, the PEGylated-Sily@ZnFe2O4. Nanocomposites may be useful in the future in sustaining a variety of tissues by lowering oxidative stress.

BackgroundXenobiotic-induced liver injury is a clinically reverent condition which may influence the development of steatohepatitis via affecting numerous pathways such as oxidative stress, inflammation, mitochondorial functioning and fatty acid biosynthesis. The current study was conducted to survey the antioxidant effect of grape seeds extract nanoparticles (GS extract NPs) against CCl4-induced oxidative stress, hepatic dysfunction and inflammatory changes.MethodsHydroethanolic Grape seed (GS) extract was prepared and characterized using high performance liquid chromatography (HPLC), inductively coupled plasma–mass spectrometry (ICP-MS) and gas chromatography–mass spectrometry (GC-MS). Then, GS extract NPs were synthesized and in vitro antioxidant, anticoagulant, cytotoxicity and anti-inflammatory testes confirmed biological activity. Finally, Twenty-five male Sprague-Dawley rats were divided into five groups (n = 5/group). Either GS extract (200 mg/kg/day) or GS extract NPs (100 mg/kg/day) were orally administrated independently to CCL4-intoxicated (0.5 ml/kg twice a week for 3 weeks) rats. Four weeks after the treatment, serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) were monitored. In addition, hepatic Malondialdehyde (MDA), Superoxide dismutases (SOD), Glutathione (GSH) and catalase (CAT) and hepatic inflammatory cytokines were assessed.ResultsGS extract NPs were spherical-shaped and regular particles (size: 16.5 to 22.5 nm and zeta potential: -39.42 mv). CCL4 -intoxicated rats showed increase of serum ALT, AST, ALP, elevation in MDA level accompanied by a decline in SOD, GSH and CAT levels in liver, compared with CCL4-untreated rats. Immunologically, serum C-Reactive Protein (CRP) and hepatic interleukin 1β (IL-1β), IL-4, IL-6 and Tumor Necrosis Factor-alpha (TNF-α) showed significant elevation, compared with CCL4 -untreated rats. Conversely, GS extract NPs supplementation potentially ameliorate hepatic functions by normalization of serum ALT, AST and ALP, reduced MDA level, improved antioxidant CAT, regulated liver inflammatory cytokines via maximal reduction of hepatic IL-1β, IL-4, IL-6 and TNF-α. ConclusionGS extract NPs augmented the antioxidant and anti-inflammatory properties of GS extract thereby protecting the liver against oxidative stress induced by CCl4 as hepatic xenobiotic.Clinical trial numberNot applicable.

Background and Aim: Nature has been a vital source of therapeutic compounds, with medicinal plants playing a key role in traditional and modern medicine. Among them, Zingiber officinale (ginger) is notable for its rich phytochemical profile and broad medicinal uses across various cultures. Ginger contains bioactive compounds like gingerols and shogaols that exhibit antioxidant, anti-inflammatory, and hepatoprotective properties. Carbon tetrachloride (CCl₄) is a known liver toxin that causes damage through oxidative stress. Accordingly, the study aimed to evaluate the hepatoprotective potential of ethanol Zinger officinale rhizome extract against carbon tetrachloride (CCl₄)-induced liver damage in Wistar rats. Methodology: A total of twenty adult Wistar rats weighing between 150–180g were randomly divided into four groups: Control, CCl₄-only, ginger-only (500mg/kg body weight), and CCl₄ + ginger (500mg/kg body weight). Following 28 days’ administration, biochemical markers of liver function (ALT, AST, ALP, TB) and oxidative stress (SOD, CAT, GPx, MDA) were evaluated. Histological assessment of liver tissues was also conducted. Results: Results revealed that CCl₄ administration significantly elevated (P<0.05) liver enzymes and lipid peroxidation while significantly reducing (P<0.05) antioxidant enzyme levels. Histological assessment also showed alterations including vacuolation and degeneration of hepatocytes in CCl₄ treated rats. However, co-administration of ginger significantly ameliorated these changes: ensuring normal liver enzyme levels, improving antioxidant defense system and preserving normal liver histoarchitecture. Conclusion: In conclusion, findings from this study show that Zingiber officinale exerts a protective effect against CCl₄-induced hepatotoxicity in Wistar rats.

Taurine ameliorates cellular senescence associated with an increased hydrogen sulfide and a decreased hepatokine, IGFBP-1, in CCl4-induced hepatotoxicity in mice.

Assessment of Nanosilymarin's Therapeutic Efficacy in Mitigating CCl4-Induced Hepatotoxicity in Rats

Mengding yellow bud polyphenols (MYBPs), as a plant active ingredient that may protect the liver, have not yet been elucidated for the potential molecular mechanism in preventing carbon tetrachloride (CCl4) induced acute liver injury (ALI) in mice. The MYBPs monomers compounds were explored by the high-performance liquid chromatography (HPLC). Mice were administered silymarin (100mg/kg b.w.) or MYBPs (50 and 100mg/kg b.w.) 2 weeks prior to CCl4-induced ALI. The liver function indexes, histopathological observation, biochemical indexes, and mRNA and protein expressions were determine. The MYBPs effectively reduced the mice liver weights, liver indexes, liver pathological injury, and the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglycerides (TG), and total cholesterol (TC). Similarly, the MYBPs decreased the interleukin (IL)-6, IL-12, tumor necrosis factor-α (TNF-α), and interferon (IFN)-γ serum levels, reduced the liver tissues myeloperoxidase (MPO) and malondialdehyde (MDA) levels, and elevated the superoxide dismutase (SOD) and glutathione (GSH) levels. The cuprozinc-superoxide dismutase (Cu/Zn-SOD), manganese-superoxide dismutase (Mn-SOD), catalase (CAT), and B-cells inhibitor-α (IκB-α) expressions markedly increased. Additionally, the MYBPs significantly decreased the nuclear factor (NF)-κB, TNF-α, IL-1 beta, inducible NOS (iNOS), and cyclooxygenase (COX)-2 expressions. HPLC showed that MYBPs contained gallic acid (GA), (-)-epigallocatechin (EGC), epigallocatechin gallate (EGCG), and (-)-epicatechin gallate (ECG). Briefly, MYBPs effectively prevented mice CCl4-induced ALI by inhibiting oxidative stress and inflammatory pathways, and its preventive effect was dose-dependent with its concentration. This study provided a scientific basis for the development of MYBPs into functional food as well as a new idea for clinical prevention and treatment of human ALI. Practical Application: MYBPs can alleviate CCl4-induced Hepatotoxicity by raising the antioxidant and antiinflammatory status and upregulating the antioxidant and antiinflammatory-related genes and protein.

Background: This study investigated the antioxidant, hepatoprotective, and sedative modulatory effects of Nigella sativa alcoholic extract (NSAE) in CCl4-induced hepatotoxicity in rats. Methods: Male Wistar rats were divided into six groups (n=6): normal control, CCl4 control, silymarin (50 mg/kg), and NSAE (100, 200, and 400 mg/kg). Hepatoprotective effects were evaluated through biochemical parameters, oxidative stress markers, and histopathological examination. Results: NSAE treatment (400 mg/kg) significantly restored liver function markers, including SGOT (20.95 ± 0.52 IU/L, p = 0.033) and SGPT (28.61 ± 0.67 IU/L, p < 0.001), compared to CCl4 control. Total protein and albumin levels were normalized to 5.68 ± 0.54 mg/dL and 3.84 ± 0.48 mg/dL, respectively. Antioxidant parameters showed marked improvement with NSAE (400 mg/kg), increasing GSH (0.26 ± 0.029 µmol/mg) and CAT (30.19 ± 2.69 µg/mL) while reducing MDA (0.048 ± 0.008 µg/mL). Histopathological examination revealed significant protection against CCl4-induced hepatic and gastric tissue damage, particularly at the 400 mg/kg. Conclusion: NSAE exhibited marked hepatoprotective activity comparable to silymarin, predominantly through antioxidant mechanisms and the maintenance of hepatic tissue integrity, indicating its potential as a natural therapeutic agent for managing liver diseases. Because of its hepatoprotective and antioxidant properties, NSAE may be explored in clinical settings as a natural supplement to traditional liver disease therapies or as a prophylactic for people at risk of liver disorders.

The study was conducted to evaluate in vitro antioxidant properties and in vivo hepatoprotective effect of the garlic extract (Allium sativum L.). Direct assessment of antioxidant activity through in vitro tests revealed that garlic extract possesses antioxidant capacity by scavenging free radicals: DPPH, ABTS•+, and hydroxyl radical (OH•-). Additionally, garlic extract also effectively inhibited the process of oxidation through chelating Fe2+. The hepatoprotective activity of the garlic extract then was evaluated in a mouse model of carbon tetrachloride (CCl4)-induced hepatotoxicity. Liver damage was induced in mice by intraperitoneal injection of 10% CCl4 at a dose of 0.5 mL/kg body weight. Garlic extract at doses of 500 and 1000 mg/kg body weight was administered for eight consecutive days prior to CCl4 administration. Silymarin suspension at a dose of 100 mg/kg body weight was used as a positive control. The present study showed that garlic extract at the tested doses significantly improved the parameters of CCl4-induced liver injury, including levels of serum transaminases (ASAT, ALAT), bilirubin, lipid peroxidation (MDA), and glutathione (GSH) (p < 0.05). The results indicated that garlic extract at doses of 500 and 1000 mg/kg body weight exhibited a hepatoprotective effect against CCl4-induced acute hepatotoxicity in mice.

Background: Kidney diseases remain a significant global health challenge, prompting researchers to explore the therapeutic potential of medicinal plants for treating various ailments, including renal disorders. This study aimed to evaluate the anti-inflammatory and antioxidant effects of the ethanolic extract of Ageratum conyzoides leaves (ESE) on kidney damage induced by carbon tetrachloride (CCl4) in a rat model. Methods: Haematological and biochemical indicators were used to evaluate the nephroprotective efficacy. Rat kidney homogenates were used to assess antioxidant and anti-inflammatory biomarkers. The histological data was used to evaluate the amount of kidney injury. Results: Pro-inflammatory cytokine expression increases brought on by CCl4 insult were dramatically and dose-dependently inhibited by ESE treatment. A significant reduction in lipid peroxidation of kidney tissue brought the concentration of defensive antioxidant enzymes to near-normal levels. The beneficial activities of ESE on CCl4-induced hepatotoxicity damage were validated by histopathological analysis of the kidney; the maximum percentage of liver protection was observed when ESE was induced at a dosage of 500 mg/kg b.wt. Conclusion: According to the findings, ESE protects the kidneys against CCl4-induced toxicity through anti-inflammatory and anti-oxidative effects. This response possibly may be due to the presence of phytochemicals.

Nasturtium officinale (N. officinale (NO)) has been widely used in traditional medicine. This study investigates the protective effects of NO against hepatic and renal damage induced by CCl4 and gentamicin, respectively, in rats. Male Wistar rats were divided into two arms: A (CCl4-induced hepatotoxicity) and B (gentamicin-induced nephrotoxicity). Seventeen groups were formed by dividing arms A and B, with nine groups in arm A and eight groups in arm B (n=5). Rats were daily treated with various doses (50, 100, and 200 mg/kg BW) of N. officinale extract (NOE) (Total extract; Oral gavage) for 14 and 28 days in arm A and B, respectively. Biochemical and histopathological evaluations and gene expression analyses were conducted on blood, liver, and kidney tissues. NOE treatment significantly modulated B-cell lymphoma protein 2 (Bcl-2)-associated X (Bax) and B-cell lymphoma protein 2 (Bcl-2) expression in kidney tissue, reducing Bax (p<0.01) and increasing Bcl-2 (p<0.05). In liver tissue, NOE inhibited tumor necrosis factor alpha (TNF-α) (p<0.01) and Interleukin-1 beta (IL-1β) (p<0.001), while reducing AST and ALT activity (p<0.001). Additionally, blood urea nitrogen (BUN) levels significantly decreased (p<0.05) in nephrotoxic rats. Our findings highlight the capability of NOE as a promising therapeutic against liver and kidney damage induced by CCl4 and gentamicin, respectively, in animal models.

The CCl4-induced hepatotoxicity model is a traditional preclinical assay applied to evaluate potential hepatoprotective compounds. However, several studies have used it with inappropriate dose and exposure time, generating both weak response or irreversible liver injury, as well as lack of representative liver and plasma biomarkers. Therefore, this study aims to determine the best dose and exposure time of CCl4 in Wistar rats, permitting a proper evaluation of potential hepatoprotective effect. Thus, CCl4-intraperitoneal doses of 0.5, 1.0, and 2.0 mL/kg were first evaluated 24 h post-exposure, and then with the best dose achieved, it was also assessed at 6 and 12 h post-exposure. The determination of the main hepatotoxicity biomarkers, including malondialdehyde (MDA), aspartate transaminase (AST), and alanine transaminase (ALT), and histopathological analyses were performed. The results suggest that 6h CCl4 post-exposure is too short to induce ideal liver injury, and at 24 h, a suggestive rat free-radical scavenger mechanism seems to revert CCl4-initiated damage. According to these data, the ideal acute CCl4-induced hepatotoxicity model was established at a dose of 2.0 mL/kg and 12 h post-exposure in Wistar rats, which demonstrated a significant increase of liver MDA levels without irreversible injury, permitting a proper and reliable evaluation of potential hepatoprotective compounds.

Evaluation of Hepatoprotective Potential of Bougainvillea spectabilis Extracts against CCl4-Induced Hepatotoxicity

There is growing interest in natural antioxidants, particularly Solanum nigrum (S. nigrum), because of their potential to protect against oxidative stress-induced organ damage and their intriguing historical use in treating various medical conditions. This pioneering study examined the unique antioxidant, hepatoprotective, and renoprotective effects of S. nigrum methanolic leaf extract on carbon tetrachloride (CCl4)-induced toxicity in albino rats. Thirty albino rats (100-120 g) were used. The 2.2 di-(4-tretoctylphenyl)-1-picrylhydrazyl radical scavenging assay was used to evaluate the antioxidant properties of S. nigrum extract. This study examined the protective effects of 150 and 300 mg/kg leaf extract against CCl4-induced toxicity. Body weight, hematological markers, and kidney and liver function were assessed. Histological analysis of liver and kidney tissue was performed. The radical scavenging activity of S. nigrum was a remarkable 85.02 ± 0.01 RSA%, compared to 66.83 ± 0.02 RSA% for gallic acid, with IC50 values of 58.3 and 1.22 μg/ml, respectively. Solanum nigrum treatment significantly decreased alanine transaminase and aspartate transaminase activities relative to CCl4-induced toxicity, a finding of significance in pharmacology and toxicology. The S. nigrum methanolic extract has an IC50 value of 58.3 μg/ml, demonstrating potent natural antioxidant properties that mitigate hepatotoxicity and renotoxicity induced by CCl4.

Enhancing the efficacy of low doses of N-acetyl-L-cysteine in mitigating CCl4-induced hepatotoxicity in animal model using physical cold plasma.

The hydroalcoholic extract of Sphaeranthus amaranthoides (Asteraceae) entire part was screened for hepatoprotective activity on carbon tetrachloride-induced hepatotoxic in Wistar rats. Plant extract was screened for phytochemicals and GC MS study was also carried out for identification of compounds. Further, hepatoprotective activity was performed where carbon tetrachloride and corn oil mixture (1:1 v/v) was injected at 2 ml/kg body weight on the 6th day. The rats were treated with hydroalcoholic extract of SA at the doses of 250 mg/kg and 500 mg /kg body weight daily for 14 days, orally. Results were compared with standard silymarin (10 mg/kg b.w). After completion of observation duration (up to 21 day), all rats were sacrificed and blood was collected. The level of biomarkers of liver injury viz. serum glutamate pyruvate transaminase (SGPT), oxaloacetate transaminase (SGOT), alkaline phosphate (ALKP), total protein (TP), total bilirubin was analysed. Further, change in body weight, liver weight, and histopathologic examination were conducted. Finally, the result concluded that SA extract is an useful therapeutic herb to prevent hepatic impairment due to the presence of various terpenoids, acid esters, phenolics, phytosterols etc. as major groups of compounds identified by GCMS in the plant.