Protection against liver ischemia–reperfusion injury in rats by silymarin or verapamil

Oliveira, Cláudia Pinto Marques Souza de; Lopasso, Fabio Pinatel; Laurindo, Francisco Rafael Martins; Leitão, Rui; Laudanna, Antônio Atílio

doi:10.1016/s0041-1345(01)02288-6

Cited by 63 publications

(47 citation statements)

References 23 publications

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“…Silymarin alone or in supplement with other drugs, can influence the therapy of many diseases of liver in many species of animals. (Oliveira et al, 2001;Sumathy et al, 2001;Kalender et al, 2005;Dehghan et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Prophylactic and Therapeutic Effects of Silymarin on Diazepam-Induced Hepatotoxicity in Cats

Mosallanejad¹

2011

American Journal of Applied Sciences

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Problem statement: Diazepam is commonly administered for seizure control and appetite stimulant in cats. Cats may develop acute fatal hepatic necrosis after receiving oral diazepam for several days. The aim of this study was to detect the protective action of silymarin on diazepam-induced hepatotoxicity in cats. Approach: About 25 healthy cats were randomly allotted to five equal groups. Animals in group A were given diazepam (repeated dose 2.5 mg kg −1 , p.o. q 12 h for 4 days); group B consisted of cats that received silymarin (30 mg kg −1 , p.o. q 12 h for 4 days) concurrent with diazepam administration; group C were received silymarin like group B, but 24 h after diazepam administration; group D were received silymarin like groups C, but 48 h after diazepam administration; group E were received silymarin like group D, but 72 h after diazepam administration. The serum concentrations of Alanine Amino Transferase (ALT), Aspartate Aminotransferase (AST), Alkaline Phosphatase (ALP), Lactate Dehydrogenase (LDH) and total and direct bilirubin were measured before diazepam administration and 24, 48, 72 and 96 h later as indices of liver injury. Results: Repeated oral administration of diazepam significantly elevated serum concentrations of ALT, AST, ALP, LDH and total and direct bilirubin in cats of group A, after 48 h. In both the groups (B and C) receiving silymarin, levels of serum enzyme activities and total and direct bilirubin remained within the normal values, but the group D and E which received silymarin 48 h and 72h later, levels of serum enzyme activities and total and direct bilirubin were increased with comparison to before diazepam administration. Conclusion: It was concluded that silymarin can protect liver tissue against oxidative stress in cats with diazepam intoxication particular in the first 24 h after exposure.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Prophylactic and Therapeutic Effects of Silymarin on Diazepam-Induced Hepatotoxicity in Cats

Mosallanejad¹

2011

American Journal of Applied Sciences

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“…Reactive oxygen species assay of lungs Superoxide ion ðO À 2 Þ in kidney tissue was measured, as described previously by Oliveira et al [27], by determining the reduction of 3 0 -{1-[(phenylamino)carbonyl]-3,4-tetrazolium}-bis(4-methoxy-6-nitro) benzenesulfonic acid hydrate (XTT) in the presence of O À 2 , with some modifications. The liver was homogenised with 2 ml of 50 mM Tris-HCl buffer (pH 7.5) and centrifuged at 5000Â g for 10 min.…”

Section: 25mentioning

confidence: 99%

The mechanism of oxidative damage in the nephrotoxicity of mice caused by nano-anatase TiO₂

Zhao

Wang

et al. 2010

Journal of Experimental Nanoscience

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While the nephrotoxicity of high-dose nano-TiO 2 has been demonstrated, very little is known about the mechanism of oxidative stress to the animal kidney. In order to understand the nephrotoxicity of nano-anatase TiO 2 particles, various biochemical and chemical parameters were assayed in mouse kidneys. Abdominal exposures of high-dose nano-anatase TiO 2 caused nephritis and oxidative stress to kidney. An increase in coefficients of the kidney, Ti accumulation and histopathological changes in kidney could be observed, followed by increased reactive oxygen species generation and lipid peroxidation, and decreased activities of superoxide dismutase, catalase, ascorbate peroxidase and total antioxidant capacity as well as antioxidants such as glutathione and ascorbic acid content. In addition, kidney functions were disrupted, including increase of the creatinine, calcium and phosphonium, and reduction of uric acid and blood urea nitrogen. Our results suggest that nephritis generation in mice caused by nano-anatase TiO 2 particles is closely related to oxidative stress.

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“…The role of silymarin in a variety of disorders in various organs like CNS, prostate, kidneys, and lung has been established (Gazak et al, 2007). Studies on humans and animals have confirmed that the natural antioxidant has no significant adverse effects (Oliveira et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Silymarin alleviates bleomycin-induced pulmonary toxicity and lipid peroxidation in mice

Razavi-Azarkhiavi

Aliomrani

Solgi

et al. 2014

Pharmaceutical Biology

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Context: The application of bleomycin is limited due to its side effects including lung toxicity. Silymarin is a flavonoid complex isolated from milk thistle [Silybum marianum L. (Asteraceae)] which has been identified as an antioxidant and anti-inflammatory compound.Objective: This study evaluates the effect of silymarin on oxidative and inflammatory parameters in the lungs of mice exposed to bleomycin. Materials and methods: BALB/c mice were divided into four groups of control, bleomycin (1.5 U/kg), bleomycin plus silymarin (50 and 100 mg/kg). After bleomycin administration, mice received 10 d intraperitoneal silymarin treatment. On 10th day, blood and lung samples were collected for measurement of oxidative and inflammatory factors. Results: Silymarin led to a decrease in lung lipid peroxidation (0.19 and 0.17 nmol/mg protein) in bleomycin-injected animals. Glutathione-S-transferase (GST) which was inhibited by bleomycin (32.4 nmol/min/mg protein) induced by higher dose of silymarin (41 nmol/min/mg protein). Silymarin caused an elevation in glutathione (GSH): 2.6 and 3.1 mmol/g lung compare with bleomycin-injected animals 1.8 mmol/g lung. Catalase (CAT) was increased due to high dose of silymarin (65.7 mmol/min/ml protein) compare with bleomycin treated-mice. Myeloperoxidase (MPO) which was induced due to bleomycin (p50.05) reduced again by high dose of silymarin (0.51 U/min/mg protein). Bleomycin led to an increase in TNF-a and interleukin-6 (IL-6) (7.9 and 11.8 pg/ml). These parameters were reduced by silymarin (p50.05). Conclusions: Silymarin attenuated bleomycin induced-pulmonary toxicity. This protective effect may be due to the ability of silymarin in keeping oxidant-antioxidant balance and regulating of inflammatory mediator release.

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Protection against liver ischemia–reperfusion injury in rats by silymarin or verapamil

Cited by 63 publications

References 23 publications

Evaluation of Prophylactic and Therapeutic Effects of Silymarin on Diazepam-Induced Hepatotoxicity in Cats

Evaluation of Prophylactic and Therapeutic Effects of Silymarin on Diazepam-Induced Hepatotoxicity in Cats

The mechanism of oxidative damage in the nephrotoxicity of mice caused by nano-anatase TiO₂

Silymarin alleviates bleomycin-induced pulmonary toxicity and lipid peroxidation in mice

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Protection against liver ischemia–reperfusion injury in rats by silymarin or verapamil

Cited by 63 publications

References 23 publications

Evaluation of Prophylactic and Therapeutic Effects of Silymarin on Diazepam-Induced Hepatotoxicity in Cats

Evaluation of Prophylactic and Therapeutic Effects of Silymarin on Diazepam-Induced Hepatotoxicity in Cats

The mechanism of oxidative damage in the nephrotoxicity of mice caused by nano-anatase TiO2

Silymarin alleviates bleomycin-induced pulmonary toxicity and lipid peroxidation in mice

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The mechanism of oxidative damage in the nephrotoxicity of mice caused by nano-anatase TiO₂