Prevention of renal ischemia–reperfusion-induced injury in rats by picroliv

Seth, Pankaj; Kumari, Ranjana; Madhavan, Subhashree; Singh, Anoop; Mani, Haresh; Banaudha, Krishna; Sharma, Shikha; Kulshreshtha, D. K.; Maheshwari, Radha K.

doi:10.1016/s0006-2952(00)00268-9

Cited by 40 publications

(25 citation statements)

References 25 publications

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“…MDA, a stable metabolite of the free radical-mediated lipid peroxidation cascade, is widely used as a marker of oxidative stress [24] . In accordance with these research studies, antioxidants recently have been found to protect renal cells from cellular injury induced by I/R [25][26][27] . Herein, renal I/R reduced SOD, CAT and GPx activities, whereas 0.6 mg/kg ivabradine exerted ameliorating effects only on SOD and CAT enzymes.…”

Section: Discussionsupporting

confidence: 67%

Dose-Dependent Protective Effect of Ivabradine against Ischemia-Reperfusion-Induced Renal Injury in Rats

Beytur

Binbay²,

Sarıhan³

et al. 2011

Kidney Blood Press Res

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Background/Aims: This study was designed to investigate the dose-dependent protective effect of ivabradine, a specific inhibitor of the cardiac sinoatrial node, on renal ischemia-reperfusion (I/R) injury in rats. Methods: Rats were divided into six groups: group 1, control; group 2, I/R (60 min ischemia followed by 24 h reperfusion); groups 3 and 4, 0.6–6 mg/kg ivabradine; and groups 5 and 6, sham+0.6–6 mg/kg ivabradine. At the end of the study, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase contents were assayed in the kidney tissues; serum blood levels of urea nitrogen (BUN), creatinine (Cr) and albumin also were determined. Results: Tissue MDA levels were found to be significantly higher in the I/R group, whereas SOD and CAT levels were lower when compared to the control group. Ivabradine (0.6 mg/kg) treatment reduced the MDA levels and elevated the SOD and CAT enzyme activity. Treatment with a dose of 6 mg/kg ivabradine further increased MDA levels and did not ameliorate SOD or CAT activities. Serum levels of BUN and Cr were significantly higher in the I/R group. I/R+0.6 mg ivabradine reduced the elevated BUN and Cr levels. Conclusion: This study indicates that ivabradine exerts a dose-dependent response beyond heart rate reduction against renal I/R injury.

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Section: Discussionsupporting

confidence: 67%

Dose-Dependent Protective Effect of Ivabradine against Ischemia-Reperfusion-Induced Renal Injury in Rats

Beytur

Binbay²,

Sarıhan³

et al. 2011

Kidney Blood Press Res

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“…PEDF is a multifunctional protein that is characterized by its broad functions, including antitumorigenicity, antimetastaticity (41,42), anti-inflammation (43), and antiangiogenicity (16) activities. Our previous study reported that circulation PEDF levels are elevated in patients with type 2 diabetes (21) and in patients with type 1 diabetes who have microvascular complications (22), while PEDF levels were decreased in renal (44) and retinal tissues (45).…”

Section: Discussionmentioning

confidence: 99%

High Levels of Pigment Epithelium–Derived Factor in Diabetes Impair Wound Healing Through Suppression of Wnt Signaling

Yang

Dai

et al. 2014

Diabetes

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Diabetic foot ulcer (DFU) caused by impaired wound healing is a common vascular complication of diabetes. The current study revealed that plasma levels of pigment epithelium-derived factor (PEDF) were elevated in type 2 diabetic patients with DFU and in db/db mice. To test whether elevated PEDF levels contribute to skin wound-healing delay in diabetes, endogenous PEDF was neutralized with an anti-PEDF antibody in db/db mice. Our results showed that neutralization of PEDF accelerated wound healing, increased angiogenesis in the wound skin, and improved the functions and numbers of endothelial progenitor cells (EPCs) in the diabetic mice. Further, PEDF-deficient mice showed higher baseline blood flow in the skin, higher density of cutaneous microvessels, increased skin thickness, improved numbers and functions of circulating EPCs, and accelerated wound healing compared with wild-type mice. Overexpression of PEDF suppressed the Wnt signaling pathway in the wound skin. Lithium chlorideinduced Wnt signaling activation downstream of the PEDF interaction site attenuated the inhibitory effect of PEDF on EPCs and rescued the wound-healing deficiency in diabetic mice. Taken together, these results suggest that elevated circulating PEDF levels contribute to impaired wound healing in the process of angiogenesis and vasculogenesis through the inhibition of Wnt/b-catenin signaling.

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“…To control the detrimental effects of ROS (especially superoxide), besides inhibiting its production, organisms have developed a variety of antioxidant defense systems, especially the endogenous antioxidant enzymes (Seth et al 2000;Wu et al 2011;Wang et al 2011), such as SOD (which dismutases superoxide to hydrogen peroxide, which represents the first step of the antioxidant pathway), hemecontaining CAT and/or the selenoenzyme GPx (which catalyses hydrogen peroxide conversion to water, which is the second step of the antioxidant pathway) (Jihen et al 2009;Kim et al 2009). In general, while GPx is more important than CAT in removing hydrogen peroxide, CAT has a predominant role at least in peroxisomes where it is concentrated (Kim et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Preventive role of gallic acid on hepatic ischemia and reperfusion injury in rats

et al. 2014

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There is little information about the hepatoprotective effects of gallic acid against ischemiareperfusion (I/R) damage. Animals were subjected to I/R. Gallic acid at doses of 50 and 100 mg/kg body weight (bw) were injected as a single dose prior to ischemia. Liver tissue homogenates were used for the measurement of malondialdehyde (MDA), catalase (CAT) and glutathione peroxidase (GPx) levels. At the same time alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were assayed in serum samples and compared statistically. While the ALT, AST, LDH activities and MDA levels were significantly increased, CAT and GPx activities significantly decreased in only I/Rinduced control rats compared to normal control rats (P \ 0.05). Treatment with gallic acid at a dose of 100 mg/kg bw significantly decreased the ALT, AST, LDH activities and MDA levels, and markedly increased activities of CAT and GPx in tissue homogenates compared to I/R-induced rats with no treatment group (P \ 0.05). In oxidative stress generated by hepatic ischemia-reperfusion, gallic acid contributes partially an alteration in the delicate balance between the scavenging capacity of antioxidant defense systems and free radicals in favour of the antioxidant defense systems in the body.

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Prevention of renal ischemia–reperfusion-induced injury in rats by picroliv

Cited by 40 publications

References 25 publications

Dose-Dependent Protective Effect of Ivabradine against Ischemia-Reperfusion-Induced Renal Injury in Rats

Dose-Dependent Protective Effect of Ivabradine against Ischemia-Reperfusion-Induced Renal Injury in Rats

High Levels of Pigment Epithelium–Derived Factor in Diabetes Impair Wound Healing Through Suppression of Wnt Signaling

Preventive role of gallic acid on hepatic ischemia and reperfusion injury in rats

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