Cardioprotective Activity of Alcoholic Extract of Tinospora cordifolia in Ischemia-Reperfusion Induced Myocardial Infarction in Rats

Rao, Pragada Rajeswara; Veeravalli, Krishna Kumar; Viswanath, Routhu Kasi; Subbaraju, Gottumukkala V.

doi:10.1248/bpb.28.2319

Cited by 108 publications

(87 citation statements)

References 29 publications

(18 reference statements)

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“…2,3,18,19,41 The discrepant effect on oxidative stress suggests that heme-catalyzed reactive species generation may differ from reactive species generated in other experimental conditions. Alternatively, silymarin-induced p53 activation could upregulate genes that encode ROS-generating enzymes (PIG 3, PIG 6) 42 or suppress antioxidant genes (MnSOD), 43 either way tipping the balance toward oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Silymarin exacerbates p53-mediated tubular apoptosis in glycerol-induced acute kidney injury in rats

2010

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Background/aims: Silymarin is an herbal extract with antioxidant properties that can reduce oxidative stressmediated injuries in murine models of liver, heart, and kidney diseases. Silymarin can also increase p53-mediated cellular apoptosis in vitro. We tested the effect of silymarin administration before glycerol-induced acute kidney injury (Gly-AKI) in rats. Methods: Renal function, tubular injury, oxidative stress, leukocytes infiltration, and renal expression of apoptosis regulating proteins (p53, p-p53, Bax, Bcl-2, survivin, and cleaved caspase-3) were evaluated 6 or 24 h after glycerol. Results: Silymarin exacerbated the renal impairment and tubular apoptosis but had no effect on tubular necrosis or renal leukocytes infiltration. Renal lipid and DNA peroxidation was increased after glycerol and silymarin did not reduce oxidative stress. Proteins p53, p-p53, and proapoptotic Bax were upregulated in Gly-AKI rats treated with silymarin, whereas anti-apoptotic Bcl-2 was reduced in this group. Cleaved caspase-3 was overexpressed in Gly-AKI rats, particularly when treated with silymarin. Survivin was less expressed in Gly-AKI than in controls, but this deficit was not aggravated by silymarin. Conclusion: The persistence of oxidative stress, inflammatory reaction, and tubular necrosis, as well as exacerbation of p53-mediated tubular apoptosis, led to a more severe renal impairment in Gly-AKI rats treated with silymarin.

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Section: Discussionmentioning

confidence: 99%

Silymarin exacerbates p53-mediated tubular apoptosis in glycerol-induced acute kidney injury in rats

2010

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“…SD rats were randomly divided into 3 groups, as follows: i) Control group rats (n=10), administered saline solution; ii) I/R group rats (n=10), receiving the aforementioned lung I/R injury and administered saline solution; iii) silymarin group rats (n=10), receiving lung I/R injury and administered 250 mg/kg/day of silymarin (Sigma-Aldrich, St. Louis, MO, USA) for 8 days (8).…”

Section: Methodsmentioning

confidence: 99%

Modulatory effect of silymarin on pulmonary vascular dysfunction through HIF-1α-iNOS following rat lung ischemia-reperfusion injury

Jin

Zhao

Zhang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Silymarin is a traditional therapeutic used to protect the liver, acting to oppose lipid peroxidation, to enhance liver regeneration and functioning as an antioxidant. However, the effects of silymarin on pulmonary vascular dysfunction have not been investigated. In the present study, the modulatory effects of silymarin on pulmonary vascular dysfunction and the underlying mechanisms behind this were investigated in a lung ischemia-reperfusion (I/R) injury rat model. Male Sprague Dawley rats were randomly divided into 3 groups, including: i) A control group (n=10); ii) an I/R group (n=10); and iii) a silymarin-treated group (n=10). All experimental rats received 250 mg/kg/day of silymarin for 8 days. Silymarin was demonstrated to markedly improve lung I/R-induced pulmonary vascular dysfunction and lung moisture. Following silymarin treatment, inflammation and oxidative stress in the lung I/R-injury rats were demonstrably suppressed. Treatment with silymarin also inhibited the activation of caspase-3 and -9, and hypoxia inducible factor-1α (HIF-1α) and inducible nitric oxide synthase (iNOS) protein expression in the lung I/R-injury rats. Silymarin was concluded to impact upon pulmonary vascular dysfunction through the HIF-1α-iNOS pathway in the lung I/R injury rat model.

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“…Rao and Viswanath 2007 [19] reported that the administration of SM before ischemia-reperfusion-induced myocardial infarction maintained the levels of marker enzymes (LDH, CK and CK-MB) compared to isoproterenol-injected rats. A possible explanation is that silymarin, via its anti-lipid peroxidation activity, causes stabilization of cardiac membranes and prevents the leakage of cardiac enzymes [32].…”

Section: Discussionmentioning

confidence: 99%

“…Silymarin has cardioprotective activity against ischemia-reperfusion induced myocardial infarction in rats [19].…”

Section: Introductionmentioning

confidence: 99%

The Cardioprotection of Silymarin in Coronary Artery Bypass Grafting Surgery

Altaei¹,

Jamal²,

Dilshad³

2013

Artery Bypass

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Cardioprotective Activity of Alcoholic Extract of Tinospora cordifolia in Ischemia-Reperfusion Induced Myocardial Infarction in Rats

Cited by 108 publications

References 29 publications

Silymarin exacerbates p53-mediated tubular apoptosis in glycerol-induced acute kidney injury in rats

Silymarin exacerbates p53-mediated tubular apoptosis in glycerol-induced acute kidney injury in rats

Modulatory effect of silymarin on pulmonary vascular dysfunction through HIF-1α-iNOS following rat lung ischemia-reperfusion injury

The Cardioprotection of Silymarin in Coronary Artery Bypass Grafting Surgery

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