Amelioration of alcohol-induced hepatotoxicity by the administration of ethanolic extract of<i>Sida cordifolia</i>Linn.

Rejitha, S.; Prathibha, P.; Indira, M.

doi:10.1017/s0007114511006568

Cited by 25 publications

(19 citation statements)

References 42 publications

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“…30 In this study also, the specific markers of liver toxicity such as GGT, ALT, and AST were elevated in serum and liver tissue of ethanol-treated group indicating the extent of hepatic injury and this was reduced to near normal levels in ethanol groups administered with either AT or AA alone. This is in agreement with earlier findings.…”

Section: Discussionsupporting

confidence: 59%

“…Primer sequences for GAPDH, CYP2E1, NF kappa B, TNFalpha, TGF beta1, and collagen were taken from the previous reports. 30,31 The PCR contained 10 mM Tris ( pH 8.3), 50 mM KCl, 1.5 mM MgCl 2 , dNTP at 20 mM each and gene specific primers at 0.5 mM each and 0.025 units/μl taq polymerase. After an initial denaturation step at 94°C, 35 amplification cycles were performed.…”

Section: Biochemical Analysismentioning

confidence: 99%

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Additive effect of alpha-tocopherol and ascorbic acid in combating ethanol-induced hepatic fibrosis

et al. 2013

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Section: Discussionsupporting

confidence: 59%

Section: Biochemical Analysismentioning

confidence: 99%

Additive effect of alpha-tocopherol and ascorbic acid in combating ethanol-induced hepatic fibrosis

et al. 2013

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“…Only the L-EF diet excessively increased plasma TG and reduced the HDL-C levels. Alcohol appears to increase the metabolic rate, causing more energy burn than storage in the body as fat in adipose tissue [32]. In reality, people eat meals consisting of a variety of foods with complex combinations of nutrients that may be synergistic [33].…”

Section: Discussionmentioning

confidence: 99%

Combination of Alcohol and Fructose Exacerbates Metabolic Imbalance in Terms of Hepatic Damage, Dyslipidemia, and Insulin Resistance in Rats

Alwahsh¹,

Xu²,

Schultze³

et al. 2014

PLoS ONE

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Although both alcohol and fructose are particularly steatogenic, their long-term effect in the development of a metabolic syndrome has not been studied in vivo. Consumption of fructose generally leads to obesity, whereas ethanol can induce liver damage in the absence of overweight. Here, Sprague-Dawley rats were fed ad libitum for 28 days on five diets: chow (control), liquid Lieber-DeCarli (LDC) diet, LDC +30%J of ethanol (L-Et) or fructose (L-Fr), and LDC combined with 30%J ethanol and 30%J fructose (L-EF). Body weight (BW) and liver weight (LW) were measured. Blood and liver samples were harvested and subjected to biochemical tests, histopathological examinations, and RT-PCR. Alcohol-containing diets substantially reduced the food intake and BW (≤3rd week), whereas fructose-fed animals had higher LW than controls (P<0.05). Additionally, leukocytes, plasma AST and leptin levels were the highest in the fructose-administered rats. Compared to the chow and LDC diets, the L-EF diet significantly elevated blood glucose, insulin, and total-cholesterol levels (also vs. the L-Et group). The albumin and Quick-test levels were the lowest, whereas ALT activity was the highest in the L-EF group. Moreover, the L-EF diet aggravated plasma triglyceride and reduced HDL-cholesterol levels more than 2.7-fold compared to the sum of the effects of the L-Et and L-Fr diets. The decreased hepatic insulin clearance in the L-EF group vs. control and LDC groups was reflected by a significantly decreased C-peptide:insulin ratio. All diets except the control caused hepatosteatosis, as evidenced by Nile red and H&E staining. Hepatic transcription of insulin receptor substrate-1/2 was mainly suppressed by the L-Fr and L-EF diets. The L-EF diet did not enhance the mitochondrial β-oxidation of fatty acids (Cpt1α and Ppar-α expressions) compared to the L-Et or L-Fr diet. Together, our data provide evidence for the coaction of ethanol and fructose with a high-fat-diet on dyslipidemia and insulin resistance-accompanied liver damage.

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“…15 The objective of the present study was to evaluate the antioxidant potential of a 50% ethanolic extract of S. cordifolia on alcohol-induced oxidative stress and to elucidate its mechanism of action.…”

Section: Introductionmentioning

confidence: 99%

Nrf2-mediated antioxidant response by ethanolic extract ofSida cordifoliaprovides protection against alcohol-induced oxidative stress in liver by upregulation of glutathione metabolism

2014

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Objective The study aimed to evaluate the antioxidant property of ethanolic extract of Sida cordifolia (SAE) on alcohol-induced oxidative stress and to elucidate its mechanism of action. Methods Male albino rats of the Sprague-Dawley strain were grouped into four: (1) control, (2) alcohol (4 g/kg body weight), (3) SAE (50 mg/100 g body weight), and (4) alcohol (4 g/kg body weight) + SAE (50 mg/100 g body weight). Alcohol and SAE were given orally each day by gastric intubation. The duration of treatment was 90 days. Results The activities of toxicity markers in liver and serum increased significantly in alcohol-treated rats and to a lesser extent in the group administered SAE + alcohol. The activity of alcohol dehydrogenase and the reactive oxygen species level were increased significantly in alcohol-treated rats but attenuated in the SAE co-administered group. Oxidative stress was increased in alcohol-treated rats as evidenced by the lowered activities of antioxidant enzymes, decreased level of reduced glutathione (GSH), increased lipid peroxidation products, and decreased expression of γ-glutamyl cysteine synthase in liver. The co-administration of SAE with alcohol almost reversed these changes. The activity of glutathione-S-transferase and translocation of Nrf2 from cytosol to nucleus in the liver was increased in both the alcohol and alcohol + SAE groups, but the maximum changes were observed in the latter group. Discussion The SAE most likely elicits its antioxidant potential by reducing oxidative stress, enhancing the translocation of Nrf2 to nucleus and thereby regulating glutathione metabolism, leading to enhanced GSH content.

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Amelioration of alcohol-induced hepatotoxicity by the administration of ethanolic extract ofSida cordifoliaLinn.

Cited by 25 publications

References 42 publications

Additive effect of alpha-tocopherol and ascorbic acid in combating ethanol-induced hepatic fibrosis

Additive effect of alpha-tocopherol and ascorbic acid in combating ethanol-induced hepatic fibrosis

Combination of Alcohol and Fructose Exacerbates Metabolic Imbalance in Terms of Hepatic Damage, Dyslipidemia, and Insulin Resistance in Rats

Nrf2-mediated antioxidant response by ethanolic extract ofSida cordifoliaprovides protection against alcohol-induced oxidative stress in liver by upregulation of glutathione metabolism

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