Protective effect of a standardized Ginkgo extract (ginaton) on renal ischemia/reperfusion injury via suppressing the activation of JNK signal pathway

Wang, Yan; Pei, Dong‐Sheng; Ji, Huai-Xue; Xing, Shu Guo

doi:10.1016/j.phymed.2008.09.003

Cited by 24 publications

(17 citation statements)

References 26 publications

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“…19 Our previous study showed that Ginaton, a new standardized antioxidant, could suppress the JNK-c-Jun-FasLcaspase 3 signaling cascade, protecting renal tubular epithelial cells against apoptosis induced by ischemia/reperfusion. 4 The current study has shown that the antioxidant selenite decreased the activation of caspase 3 and caspase 3 substrate PARP induced by ischemia/reperfusion, which might take effect at the final step of the apoptotic cascade.…”

Section: Discussionmentioning

confidence: 59%

“…1,2 ROS-induced cell injury has been attributed, in part, to changes in activation of intracellular signaling molecules, including the mitogen-activated protein kinase (MAPK) family. 3,4 Apoptosis signal regulating kinase 1 (ASK1) is a general mediator of cell death in response to a variety of stimuli, including oxidative stress and chemotherapeutic drugs such as cisplatin and paclitaxel. 5,6 ASK1 activates both the MKK3/MKK6-p38 signaling cascades and MKK4/MKK7-c-jun N-terminal kinase (JNK).…”

Section: Introductionmentioning

confidence: 99%

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Protective effect of selenite on renal ischemia/reperfusion injury through inhibiting ASK1–MKK3–p38 signal pathway

Wang

Ji²,

Zheng³

et al. 2009

Redox Report

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Previous studies have reported that selenite, a known antioxidant, protects brain against ischemia/reperfusion injury, which is mediated by oxidative stress. The aim of this study was to investigate whether selenite can protect kidney against ischemic injury by reducing activation of the apoptosis signal regulating kinase 1 (ASK1)/mitogen-activated protein kinase kinase 3 (MKK3)/p38 mitogen-activated protein kinase signaling pathway. The activation and expression of ASK1, MKK3, p38, caspase 3 and cleaved PARP were analyzed by Western blot. Apoptosis of renal tubular epithelial cells was assessed by the terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling method. Malondialdehyde (MDA) levels were measured by the thiobarbituric acid reaction. Blood serum creatinine and blood urea nitrogen level were measured with an Olympus automatic multi-analyzer. We found that selenite attenuated significantly ASK1, MKK3, and p38 phosphorylation at 3 h after renal ischemia. Furthermore, selenite decreased significantly renal epithelial tubular cell apoptosis. In addition, selenite reduced the MDA level. These findings suggest that the protective action of selenite on ischemia renal injury is associated closely with reducing activation of the ASK1-MKK3-p38 signal pathway.

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Section: Discussionmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Protective effect of selenite on renal ischemia/reperfusion injury through inhibiting ASK1–MKK3–p38 signal pathway

Wang

Ji²,

Zheng³

et al. 2009

Redox Report

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“…Similarly, Radix Codonopsis and the extract saponins increased superoxide dismutase (SOD) level and decreased apoptosis index in a model of kidney transplantation (He et al, 2011), artemisia asiatica extract increased the level of HO-1 and Bcl-2 in the setting of acute renal IRI damage (Jang et al, 2015), and Ginkgo extract (ginaton) was shown to possess anti-oxidation and anti-inflammation activities through suppressing extrinsic apoptotic signal pathway induced by c-Jun N-terminal kinase (JNK) signal pathway (Wang et al, 2008). …”

Section: Herbs Food and Dietary Nutrientsmentioning

confidence: 99%

Renoprotective approaches and strategies in acute kidney injury

Yang

Song

et al. 2016

Pharmacology & Therapeutics

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Acute kidney injury (AKI) is a major renal disease associated with a high mortality rate and increasing prevalence. Decades of research has suggested numerous chemical and biological agents with beneficial effects in AKI. In addition, cell therapy and molecular targeting have been explored for reducing kidney tissue damage and promoting kidney repair or recovery from AKI. Mechanistically, these approaches may mitigate oxidative stress, inflammation, cell death, and mitochondrial and other organellar damage, or activate cytoprotective mechanisms such as autophagy and pro-survival factors. However, none of these findings has been successfully translated into clinical treatment of AKI. In this review, we analyze these findings and propose experimental strategies for the identification of renoprotective agents or methods with clinical potential. Moreover, we propose the consideration of combination therapy by targeting multiple targets in AKI.

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“…The surgical technique was followed as previously described [21] . Following urethane anesthesia (1.6 g/kg i.p.…”

Section: Surgical Proceduresmentioning

confidence: 99%

Nephroprotective Effect of Telmisartan in Rats with Ischemia/Reperfusion Renal Injury

Fouad¹,

Qureshi²,

Al-Sultan³

et al. 2010

Pharmacology

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We investigated the protective effect of telmisartan, an angiotensin II receptor antagonist, against ischemia/reperfusion renal injury in rats. Bilateral ischemia was induced by clamping both renal vascular pedicles for 45 min followed by reperfusion for 3 h. Untreated rats exposed to ischemia/reperfusion showed significant elevations in blood urea nitrogen and serum creatinine levels, renal tissue levels of malondialdehyde, tumor necrosis factor-α and nitric oxide, and caspase-3 activity. This was associated with significant decreases in renal reduced glutathione level, catalase and superoxide dismutase activities. Also, significant increases in serum and renal tissue levels of homocysteine were detected following ischemia/reperfusion. Pre-ischemic treatment with telmisartan (0.3 mg/kg/day, i.p.) for 7 consecutive days significantly attenuated the increases in blood urea nitrogen, serum creatinine, renal malondialdehyde, tumor necrosis factor-α, nitric oxide, caspase-3 activity, and serum and renal homocysteine levels, and significantly restored the renal antioxidant defenses. In addition, light and electron microscopic examinations revealed that telmisartan pre-treatment markedly ameliorated ischemia/reperfusion-induced renal tissue damage. It was concluded that telmisartan, through its antioxidant, anti-inflammatory and antiapoptotic effects, can be considered a potential candidate to protect against acute ischemia/reperfusion renal injury.

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Protective effect of a standardized Ginkgo extract (ginaton) on renal ischemia/reperfusion injury via suppressing the activation of JNK signal pathway

Cited by 24 publications

References 26 publications

Protective effect of selenite on renal ischemia/reperfusion injury through inhibiting ASK1–MKK3–p38 signal pathway

Protective effect of selenite on renal ischemia/reperfusion injury through inhibiting ASK1–MKK3–p38 signal pathway

Renoprotective approaches and strategies in acute kidney injury

Nephroprotective Effect of Telmisartan in Rats with Ischemia/Reperfusion Renal Injury

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