Pharmacognostic evaluation and hepatoprotective activity of Solanum americanum.

The prophylactic effects of oleanolic acid (OA) isolated from chloroform extract (CE) of Flaveria trinervia against ethanol induced liver toxicity was investigated using rats. CE and OA at three different doses were tested by administering orally to the ethanol treated animals during the last week of the 7 weeks study. Silymarin was used as the standard reference. The substantially elevated serum enzymatic levels of serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, alkaline phosphatase and bilirubin in ethanol treated animals were restored towards normalcy by treatment of CE and OA. In vivo antioxidant and in vitro free radical scavenging activities were also positive for all the three concentrations of CE and OA. However, OA at 150 mg/kg showed significant activity when compared to the other two doses. Biochemical observations in support with histopathological examinations revealed that CE and OA possess hepatoprotective action against ethanol induced hepatotoxicity in rats.

Objective: To evaluate the ethanol extract of Voacanga grandifolia for hepatoprotective and antioxidant potential against ethanolinduced liver toxicity in rats. Methods: Sprague-Dawley rats were administered ethanol (7 g/kg) and then treated with 100 and 200 mg/kg of Voacanga grandifolia extract. The phytochemical constituents and antioxidant potential of Voacanga grandifolia extract were evaluated by GC-MS and in vitro antioxidant assays. Biochemical indicators for liver damage and proapoptotic and antiapoptotic gene expression were determined using biochemical kits, ELISA, and qRT-PCR, respectively. Additionally, histopathological study of the liver was performed. Results: GC-MS identified propanoic acid, meso-erythritol, D-pinitol, myo-inositol, and hexadecanoic acid in Voacanga grandifolia extract. Voacanga grandifolia extract (100 and 200 mg/kg) increased the concentration of enzymatic antioxidants while diminishing the levels of inflammatory cytokines and biochemical indicators. qRT-PCR assay showed that Voacanga grandifolia extracts upregulated antiapoptotic gene expression while downregulating pro-apoptotic gene expression. Furthermore, the plant extract improved the hepatic architecture of ethanol-intoxicated rats. Conclusions: Voacanga grandifolia extract demonstrates hepatoprotective activity against alcohol-induced liver injury in rats and could be a potential hepatoprotective agent.

Hepatoprotective potential of Diospyros melanoxylon (Roxb.) leaf extract by inhibition of IL-6, COX-2, and 5-LOX expression in paracetamol intoxicated rats.

Plants play an important role in the life of human, as the major source of food, as well as for the maintenance and improvement of health and for the elimination of the enemies since ages. Plants are the basic source of knowledge of modern medicine. The present study was conducted to evaluate the hepatoprotective activity of ethanolic leaves extract of Avicennia marina are evaluated in alcohol induced hepatotoxicity in rats. Silymarin (100mg/kg) was given as reference standard. The ethanolic leaves extract of Avicennia marina have shown very significant hepatoprotection against alcohol induced hepatotoxicity in albino rats in reducing SGOT, SGPT, Alkaline phosphatase (ALP) and GGT and levels of total bilirubin and total protein were investigated and showed an increase in alcohol induced rats when compared to control. The extracts of the test plant exhibited significant (p < 0.01) hepatoprotective activity against the alcohol induced liver models by improving liver function which was indicated by reduction in the levels of SGOT, SGPT, ALP, GGT, total bilirubin and total protein. Keywords: Avicennia marina, Hepatoprotective, Liver Enzymes, Silymarin

Scientists around the world are focusing on 'green,' environmentfriendly, and cost-effective green synthesis of nanometals using various plant extracts to combat various ailments. Among nanometals, Silver (Ag) is one of the most commercialised nanomaterials due to its wide applications in biotechnology and biomedical fields. The present study reports the first facile synthesis, characterization, and process optimisation of Ag nanoparticles (NPs) using aqueous Grewia tiliaefolia leaf extract (Gt) as a reducing and surface functionalising agent. Characterisation of Gt-mediated Ag-NPs was performed using FTIR. The morphology and microstructures of Gt-derived Ag-NPs were analysed using TEM and FE-SEM. In vitro, antioxidant activity was evaluated against DPPH radicals, hydrogen peroxide radicals, and ferric ions. In vitro, anticancer activity was assessed on MCF-7 and HepG2 cell lines. In vivo, hepatoprotective activity was tested against paracetamol-induced liver toxicity in rats. FTIR analysis confirmed the interaction between Ag-NPs and Gt. The optimal conditions for Gt-derived Ag-NPs were found to be 4 mM AgNO3, 5% Gt, at 90°C for 60 minutes, at pH 9. UV-Visible spectroscopy, XRD, FE-SEM, and TEM revealed the phase formation, spherical morphology, and surface functionalisation of Gt-derived Ag-NPs, which were stable (-28.3 mV) with an average particle size of 14.5±0.05 nm. The Gt-derived Ag-NPs were found to be highly effective in significantly inhibiting DPPH radical, ferric ions, and hydroxyl radicals. Additionally, the cytotoxicity of Gt-derived Ag-NPs was more effective against MCF-7 cells compared to HepG2 cells. They also exhibited dose-dependent protection against hepatoprotective activity in albino rats. The hepatoprotective effects of Gt-mediated Ag-NPs likely result from the combined action of bioactive phytochemicals (such as α/β-amyrin, γ-lactones, betulin, and lupeol), and their ability to scavenge ROS, reduce oxidative stress, and modulate inflammatory pathways. These mechanisms, supported by reduced lipid peroxidation and increased antioxidant activity in paracetamol-induced hepatotoxicity, suggest their therapeutic potential in liver protection and regeneration. Overall, Gt proves to be an eco-friendly and non-toxic source for synthesizing bioactive Ag-NPs at optimal conditions.

Anogeissus acuminata is used to treat wounds, diarrhoea, dysentery, and skin ailments. However, its hepatoprotective effect against ethanol-induced liver damage is yet to be reported. The phenolic-enriched ethyl acetate fraction of Anogeissus acuminata (AAE) was evaluated for hepatoprotective activity against ethanol-induced liver toxicity in rats. The intoxicated animals were treated with a phenolic-rich fraction of Anogeissus acuminata (AAE) (100 and 200 mg/kg) and silymarin (100 mg/kg). The antioxidant activity of AAE was analysed. Biochemical markers (ALT, AST, ALP, GGT, and TBL) for liver injury in ethanol-administered animals resulted in higher levels of key serum biochemical injury markers, as evidenced by increased levels of ALT (127.24 ± 3.95), AST (189.54 ± 7.56), ALP (263.88 ± 12.96), GGT (91.65 ± 3.96), and TBL (2.85 ± 0.12) compared to Group I ALT (38.67 ± 3.84), AST (64.45 ± 5.97), GGT (38.67 ± 3.84), and TBL (0.53 ± 064) (p < 0.05). AAE administration decreased serum biochemical liver injury markers as manifested in Group III animals’ ALT (79.56 ± 5.16), AST (151.76 ± 6.16), ALP (184.67 ± 10.12), GGT (68.24 ± 4.05), TBL (1.66 ± 0.082) (p < 0.05), and Group IV ALT (55.54 ± 4.35), AST (78.79 ± 4.88), ALP (81.96 ± 9.43), GGT (47.32 ± 2.95), TBL (0.74 ± 0.075) (p < 0.05). Group IV exhibited the most significant reduction in serum biochemical markers as compared to Group III (p < 0.05) and close to silymarin-treated Group V ALT (44.42 ± 3.15), AST (74.45 ± 5.75), ALP (67.32 ± 9.14), GGT (42.43 ± 2.54), TBL (0.634 ± 0.077). Gene expression indices and histoarchitecture were evaluated to demonstrate the potential of AAE. The bioactive fraction of Anogeissus acuminata was rich in phenolics and flavonoid content. GC–MS analysis identified gallic acid, palmitic acid, cis-10-heptadecenoic acid, 9-octadecenoic acid, epigallocatechin, 2,5-dihydroxyacetophenone, and catechin. Oral administration of AAE (100 and 200 mg/kg) lowered the elevated levels of the biochemical markers and interleukin, and enhanced the level of enzymatic antioxidant. It also downregulated the expression level of proapoptotic genes and upregulated the expression level of the antiapoptotic gene along with improved liver histopathology.

Curcuma xanthorrhiza is widely used in Indonesia folk medicine to treat liver disorders. This study has evaluated the hepatoprotective activity of standardized ethanolic extract of C. xanthorrhiza. The extract was standardized using GC-MS. The hepatoprotective activity of this extract was studied using ethanolinduced liver toxicity in rats. This respective activity was assessed through monitoring liver function tests through the measurement of alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP) and protein content. Further, hepatic tissues were also subjected to histopathological studies. Pretreatment of the standardized C. xanthorrhiza ethanolic extract (500 mg/kg) reduced the fatty liver symptoms and significantly (p < 0.05) inhibit the increase of respective serum enzyme levels. The results of the present study indicated that C. xanthorrhiza possess hepatoprotective effects which could act as an effective treatment for acute hepatic diseases.

Background: Titanium dioxide nanoparticles (TiO2 NPs) were healthy well-known as a photocatalyst and it was extensively utilized for photocatalysed corrosion, sensor essentials, water distillation and had numerous other submission. Also, in food industry. However they also had poisonous result on animals uncovered to them. Objectives: we examined the probable ameliorative result for the two flavonoids morin and rutin which had apotent antioxidant activity, against TiO2 nanoparticles-induced toxicities in rat liver. Materials and methods: Albino rats (n =70, weight 150-200g) were divided into seven groups. Group (G1) (control), G2 (treated with morin 30 mg/kg), G3 (treated with rutin 80 mg/kg), G4 (toxic group that administrated orally with titanium dioxide nanoparticles 100 mg/kg), G5 (TiO2 NPs+ morin), G6 (TiO2 NPs+ rutin), G7 (TiO2 NPs+ morin+ rutin). The evaluated parameters included liver function markers, some minerals and electrolytes, antioxidant (superoxide dismutase SOD, catalase CAT and glutathione GSH) and oxidative stress malondialdehyde (MDA) biomarkers in addition to DNA fragmentation and histopathological examination of liver tissues. Results: These experimental study showed that a significant increase of serum ALT, AST, ALP activities. Also, serum potassium (K) and phosphorous (P) levels, hepatic MDA content, comet, tail length, DNA in tail and tail moment of DNA fragmentation were detected in TiO2 NPs (G4) group indicating liver damage which compared with control group (G1) but this parameters decreased significantly in morin (G5) or rutin (G6) when compared with toxic group (G4), in combination group (TiO2 NPs+ morin+ rutin) (G7) succeeded to decrease significantly in this parameters and returns to (G1). Also, our results showed that a significant decrease in total protein, albumin, sodium (Na), calcium (Ca) levels, glutathione (GSH) level, superoxide dismutase (SOD) and catalase (CAT) activities in toxic groups (G4) but succeeded to increase significantly in this parameters in G5, G6 and G7 in compared with control group and restore it. Conclusion: TiO2NPs oral administration induced toxic effects and DNA damage in the liver that may be attributable to oxidative stress.Also, administration of morin and/or rutin with TiO2NPs offers protection against their damaging effect.

Objective: To evaluate the hepatoprotective effect of Prunus armeniaca L. (Apricot) leaf on paracetamol induced liver toxicity in rats. Method: Phytochemical investigation was performed to find active constituents of the plant extracts by the different phytochemical tests. After induction of liver toxicity, the biochemical parameters such as serum glutamic pyruvic transaminase (sGPT), serum glutamic oxaloacetic transaminase (sGOT), serum alkaline phosphatase (sALP), serum bilirubin (SB), thiobarbituric acid reactive substances (TBARS), γ-glutamyl transferase (GGT), lactate dehydrogenase (LDH), total protein (TP), albumin. The physical parameters including liver weight, body weight and histopathological changes in the liver were studied with Ursodeoxycholic acid as standard hepatoprotective agents. Results: The phytochemical investigation of the extracts showed the presence of Alkaloids, volatile oil, saponin glycosides, condensed tanins, terpenoids, steroids and flavonoids. Methanol and aqueous extract before the paracetamol administration caused a significant reduction in the values of sGOT, sGPT, sALP, TBARS, GGT, LDH TP, Albumin and sB (P<0.01) almost comparable to the Ursodeoxycholic acid. The hepatoprotective activity was confirmed by histopathological examination of the liver tissue of control and treated animals. Conclusions: The result concludes that Prunus armeniaca L. possesses the hepatoprotective effect against paracetamol induced liver toxicity in rats.

BackgroundDecoction prepared from leaves of Atalantia ceylanica is used in traditional medicine in Sri Lanka for the treatment of various liver ailments since ancient times. Lyophilized powder of the water extract of A. ceylanica leaves was investigated for its phytochemical constituents, antioxidant and hepatoprotective activity in-vitro.MethodsThe total phenolic and flavonoid contents were determined using Folin Ciocalteu method and aluminium chloride colorimetric assay respectively. The antioxidant activities of the decoction were investigated using 1,1-Diphenyl-2-picrylhydrazyl (DPPH), hydroxyl radical, nitric oxide scavenging assays and ferric ion reducing power assay. Hepatotoxicity was induced on porcine liver slices with ethanol to study hepatoprotective activity. Porcine liver slices were incubated at 37°C with different concentrations of the water extract of A. ceylanica in the presence of ethanol for 2 hours. The hepatoprotective effects were quantified by the leakage of alanine transaminase (ALT), aspartate transaminase (AST) and lactate dehydrogenase (LDH) to the medium. Thiobarbituric acid reactive substances (TBARS) assay was performed to examine the anti-lipid peroxidation activity caused by the plant extract.ResultsThe mean ± SD (n =9) for the levels of total phenolics and flavonoids were 4.87 ± 0.89 w/w% of gallic acid equivalents and 16.48 ± 0.63 w/w% of (-)-Epigallocatechin gallate equivalents respectively. The decoction demonstrated high antioxidant activity. The mean ± SD values of EC50 were 131.2 ± 36.1, 48.4 ± 12.1, 263.5 ± 28.3 and 87.70 ± 6.06 μg/ml for DPPH, hydroxyl radical, nitric oxide scavenging assays and ferric ion reducing power assay respectively.A significant decrease (p <0.05) was observed in ALT, AST and LDH release from porcine liver slices treated with A. ceylanica extract at a concentration of 2 mg/ml in the presence of ethanol (5 M) compared to that of ethanol (5 M) treated slices. Furthermore, a reduction in lipid peroxidation was also observed in liver slices treated with the leaf extract of A. ceylanica (2 mg/ml) compared to that of ethanol induced liver toxicity (p <0.05).ConclusionsThe results suggest that aqueous extract of A. ceylanica exerts hepatoprotective activity against ethanol induced liver toxicity of porcine liver slices which can be attributed to the antioxidant properties possessed by the plant material.Electronic supplementary materialThe online version of this article (doi:10.1186/1472-6882-14-395) contains supplementary material, which is available to authorized users.

Objective- Hepatoprotective activity of Chenopodium album leaves extract in CCl 4 induced hepatotoxicity in rats. Method- The present study has been undertaken to evaluate hepatoprotective activity of Chenopodium album leaves extract in CCl 4 induced hepatotoxicity in rats. The study was carried out by comparing SGOT, SGPT, Alkaline Phosphate, Direct Bilirubin, Total Bilirubin and Total proteins level in serum of different groups of rats. Histopathological study was also done on liver tissue of the all group of animals and compared with standard, positive control and negative control groups. Result - Rats treated with Chenopodium album leave extract caused a significant reduction in SGOT, SGPT, Alkaline phosphate, direct bilirubin, total bilirubin. Level of total proteins was found retrieving towards normalcy. Level of these enzymes was almost comparable to standard drug i.e. Silymarin. Hepatoprotective activity was confirmed by histopathological study of liver tissue of control and treated animals. Conclusion - From results it can be concluded that Chenopodium album possess hepatoprotective activity against CCl 4­ induced liver toxicity in rats.

We compared the preventive capacity of high intakes of vitamin C (VC) and vitamin E (VE) on oxidative stress and liver toxicity in rats fed a low-fat ethanol diet. Thirty-two Wistar rats received the low fat (10% of total calories) Lieber-DeCarli liquid diet as follows: either ethanol alone (Alc group, 36% of total calories) or ethanol in combination with VC (Alc + VC group, 40 mg VC/100 g body weight) or VE (Alc + VE group, 0.8 mg VE/100 g body weight). Control rats were pair-fed a liquid diet with the Alc group. Ethanol administration induced a modest increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST), conjugated dienes (CD), and triglycerides but decreased total radical-trapping antioxidant potential (TRAP) in plasma. VE supplementation to alcohol-fed rats restored the plasma levels of AST, CD, and TRAP to control levels. However, VC supplementation did not significantly influence plasma ALT, AST, or CD. In addition, a significant increase in plasma aminothiols such as homocysteine and cysteine was observed in the Alc group, but cysteinylglycine and glutathione (GSH) did not change by ethanol feeding. Supplementing alcohol-fed rats with VC increased plasma GSH and hepatic S-adenosylmethionine, but plasma levels of aminothiols, except GSH, were not influenced by either VC or VE supplementation in ethanol-fed rats. These results indicate that a low-fat ethanol diet induces oxidative stress and consequent liver toxicity similar to a high-fat ethanol diet and that VE supplementation has a protective effect on ethanol-induced oxidative stress and liver toxicity.

Alcohol consumption is associated with several health issues, including Alcoholic Liver Disease (ALD). Quinic acid, a cyclic polyol compound, is known for its antioxidant, anticancer, anti-inflammatory, and hepatoprotective properties. This study aims to elucidate the protective mechanisms of quinic acid against ethanol-induced liver toxicity in rats. Male rats (n=32) were divided into four groups (n=8 per group) and treated over 60 days. Group 1 received a standard diet with isocaloric glucose; Group 2 was treated with 30% ethanol daily; Group 3 received 30% ethanol and quinic acid (50 mg/kg) from day 31; Group 4 was given glucose and quinic acid from day 31. Biochemical, physiological, and histological evaluations were performed post-treatment. Ethanol-treated rats exhibited significant decreases in body weight, abnormal liver morphology, increased liver enzyme levels (AST, ALT, ALP, and GGT), disrupted lipid and renal profiles, and altered phase I and II enzyme activities. Quinic acid supplementation in ethanol-treated rats significantly reversed these changes by improving body weight, restoring liver morphology, normalizing liver enzyme activities, and maintaining lipid-lipoprotein balance and enzyme levels. Histopathological analysis demonstrated reduced liver damage in quinic acid-treated groups. Quinic acid exhibits hepatoprotective effects against ethanol-induced toxicity by reducing oxidative stress, normalizing liver functions, and preserving liver structure. These findings highlight its potential as a therapeutic agent for managing ALD.

In the present study, preventive and protective effects of Ocimum gratissimum in ethanol-induced hepatotoxicity are assessed in albino rats. A methanol extract of O. gratissimum leaves is prepared, with a yield of 3.5% (w/w) of the dry weight of leaves. Graded doses of the extract (10, 20, 40 and 80 mg/kg body weight), together with ethanol (5 gm/kg body weight) are administered orally to experimental groups for 30 days. Normal control rats receive distilled water only, while rats in an alcohol control group (AC) receive ethanol only for 30 days. O. gratissimum reduced the level of thiobarbituric acid reactive substance in all experimental groups (E1–E4). Alanine transaminase and aspartate transaminase levels fell in all experimental groups (E1–E4), but this reduction was significant only in groups E3 and E4 (P<0.05), indicating inhibition of lipid peroxidation by free radicals generated after ethanol metabolism. Levels of antioxidants also increased. Ascorbic acid and glutathione levels increased in all experimental groups (E1–E4; P<0.05 and P<0.01, respectively). A significant increase in catalase (P<0.05) was noted only in group E4, although an upward trend was noted in all experimental groups. This study shows that O. gratissimum prevents free radical damage to the liver and thus protects the organ from oxidative stress.

Protective effects of Phyllanthus acidus (L.) Skeels leaf extracts on acetaminophen and thioacetamide induced hepatic injuries in Wistar rats