The antioxidant role of N-acetylcysteine on the testicular remote injury after skeletal muscle ischemia and reperfusion in rats

Takhtfooladi, Mohammad Ashrafzadeh; Jahanshahi, Amirali; Sotoudeh, Ahmad; Khansari, Mohammadreza; Takhtfooladi, Hamed Ashrafzadeh

doi:10.5114/pjp.2013.38140

Cited by 17 publications

(17 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The role of oxidative stress in the setting of hind limb I/R injury is well demonstrated in previous studies [27–29]. Hence, we investigated the effects of ScB on the level of MDA and SOD activity.…”

Section: Discussionmentioning

confidence: 78%

Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

Zhu

Cai

Zhou

et al. 2017

BioMed Research International

View full text Add to dashboard Cite

Schisandrin B (ScB), isolated from Schisandra chinensis (S. chinensis), is a traditional Chinese medicine with proven cardioprotective and neuroprotective effects. However, it is unclear whether ScB also has beneficial effects on rat hind limb ischemia/reperfusion (I/R) injury model. In this study, ScB (20 mg/kg, 40 mg/kg, and 80 mg/kg) was administered via oral gavage once daily for 5 days before the surgery. After 6 h ischemia and 24 h reperfusion of left hind limb, ScB reduced I/R induced histological changes and edema. ScB also suppressed the oxidative stress through decreasing MDA level and increasing SOD activity. Moreover, above changes were associated with downregulated TNF-α mRNA expression and reduced level of IL-1β in plasma. Meanwhile, ScB treatment downregulated activation of p38MAPK, ERK1/2, and NF-κB in ischemic skeletal muscle. These results demonstrate that ScB treatment could prevent hind limb I/R skeletal muscle injury possibly by attenuating oxidative stress and inflammation via p38MAPK, ERK1/2, and NF-κB pathways.

show abstract

Section: Discussionmentioning

confidence: 78%

Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

Zhu

Cai

Zhou

et al. 2017

BioMed Research International

View full text Add to dashboard Cite

show abstract

“…To determine whether ROS mediated the activation of CaMKII, NAC (150 mg·kg −1 , i.v.) was injected immediately prior to occlusion (Takhtfooladi et al ., ). The expression of ox‐CaMKII and p‐CaMKII were similar in the sham‐ and NAC‐treated animals ( P > 0.05; Figure B).…”

Section: Resultsmentioning

confidence: 97%

Activation of M₃ cholinoceptors attenuates vascular injury after ischaemia/reperfusion by inhibiting the Ca²⁺/calmodulin‐dependent protein kinase II pathway

et al. 2015

British J Pharmacology

View full text Add to dashboard Cite

Background and Purpose The activation of M3 cholinoceptors (M3 receptors) by choline reduces cardiovascular risk, but it is unclear whether these receptors can regulate ischaemia/reperfusion (I/R)‐induced vascular injury. Thus, the primary goal of the present study was to explore the effects of choline on the function of mesenteric arteries following I/R, with a major focus on Ca2+/calmodulin‐dependent protein kinase II (CaMKII) regulation. Experimental Approach Rats were given choline (10 mg·kg−1, i.v.) and then the superior mesenteric artery was occluded for 60 min (ischaemia), followed by 90 min of reperfusion. The M3 receptor antagonist, 4‐diphenylacetoxy‐N‐methylpiperidine methiodide (4‐DAMP), was injected (0.12 μg·kg−1, i.v.) 5 min prior to choline treatment. Vascular function was examined in rings of mesenteric arteries isolated after the reperfusion procedure. Vascular superoxide anion production, CaMKII and the levels of Ca2+‐cycling proteins were also assessed. Key Results Choline treatment attenuated I/R‐induced vascular dysfunction, blocked elevations in the levels of reactive oxygen species (ROS) and decreased the up‐regulated expression of oxidised CaMKII and phosphorylated CaMKII. In addition, choline reversed the abnormal expression of Ca2+‐cycling proteins, including Na+/Ca2+ exchanger, inositol 1,4,5‐trisphosphate receptor, sarcoplasmic reticulum Ca2+‐ATPase and phospholamban. All of these cholinergic effects of choline were abolished by 4‐DAMP. Conclusions and Implications Our data suggest that inhibition of the ROS‐mediated CaMKII pathway and modulation of Ca2+‐cycling proteins may be novel mechanisms underlying choline‐induced vascular protection. These results represent a significant addition to the understanding of the pharmacological roles of M3 receptors in the vasculature, providing a new therapeutic strategy for I/R‐induced vascular injury. Linked Articles This article is part of a themed section on Chinese Innovation in Cardiovascular Drug Discovery. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-23

show abstract

“…The first phase occurs immediately after reperfusion, extends for a few hours and is a typical oxidative stress situation, reversible in terms of cellular injury 2,8 . MDA is the end product of lipid peroxidation and is a well-known parameter for determining the increased free radical formation in post-ischemic tissue 22,23 . SOD and glutathione peroxidase are major enzymes that scavenge harmful ROS in male reproductive organs 24 .…”

Section: Discussionmentioning

confidence: 99%

Protective effect of metformin on testicular ischemia/reperfusion injury in rats

et al. 2016

View full text Add to dashboard Cite

PURPOSE:To investigate the protective effect of metformin on testicular ischemia/reperfusion (I/R) injury in rats. METHODS:Eighteen adult male Wistar rats were randomly divided into three experimental groups (n=6), as follows: Sham, I/R, and Metformin. 1-hour ischemia was induced by the left testicular artery and vein clipping followed by 7 days of reperfusion. Metformin (100 mg/kg) was administrated orally for 7 days via oral gavage after ischemic period. At the end of trial, the left testis was removed for histological analysis and oxidative stress measurement.RESULTS: I/R reduced superoxide dismutase (SOD) activities and testicular Johnsen's scores accompanied by an elevation in malondialdehyde (MDA) and myeloperoxidase (MPO) levels in comparison with the sham group (P < 0.05). Compared to I/R group, metformin restored testicular Johnsen's scores, SOD activity, MDA and MPO levels (P < 0.05). CONCLUSION:Metformin has a protective effect against I/R injury on the testis.

show abstract

The antioxidant role of N-acetylcysteine on the testicular remote injury after skeletal muscle ischemia and reperfusion in rats

Cited by 17 publications

References 36 publications

Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

Activation of M₃ cholinoceptors attenuates vascular injury after ischaemia/reperfusion by inhibiting the Ca²⁺/calmodulin‐dependent protein kinase II pathway

Protective effect of metformin on testicular ischemia/reperfusion injury in rats

Contact Info

Product

Resources

About

The antioxidant role of N-acetylcysteine on the testicular remote injury after skeletal muscle ischemia and reperfusion in rats

Cited by 17 publications

References 36 publications

Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

Activation of M3 cholinoceptors attenuates vascular injury after ischaemia/reperfusion by inhibiting the Ca2+/calmodulin‐dependent protein kinase II pathway

Protective effect of metformin on testicular ischemia/reperfusion injury in rats

Contact Info

Product

Resources

About

Activation of M₃ cholinoceptors attenuates vascular injury after ischaemia/reperfusion by inhibiting the Ca²⁺/calmodulin‐dependent protein kinase II pathway