TRPV1 Agonist Capsaicin Attenuates Lung Ischemia-Reperfusion Injury in Rabbits

Wang, Maohua; Ji, Peng; Wang, Rurong; Zhao, Lifang; Xia, Zhengyuan

doi:10.1016/j.jss.2010.08.053

Cited by 40 publications

(34 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ROS are highly reactive and could react with lipid component of cell membrane [5]. Therefore, detection of oxidative products of lipid peroxidation has been widely used to estimate overall status of oxidative damage [14]. In the present study, we observed that reperfusion to the ischemic lung increased oxidative product MDA contents and decreased endogenous antioxidant enzyme SOD activities in lung tissues at the end of reperfusion.…”

Section: Discussionsupporting

confidence: 53%

Hydrogen-Rich Saline Attenuates Lung Ischemia-Reperfusion Injury in Rabbits

Zhou

Liu

et al. 2012

Journal of Surgical Research

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 53%

Hydrogen-Rich Saline Attenuates Lung Ischemia-Reperfusion Injury in Rabbits

Zhou

Liu

et al. 2012

Journal of Surgical Research

View full text Add to dashboard Cite

“…On the other hand, the protective effect of capsaicin against ischemia/reperfusion injury in the heart (Wang and Wang, 2005), lung (Wang et al, 2012) and kidney (Ueda et al, 2008) has been reported. In spontaneously hypertensive rats, dietary intake of capsaicin (0.02%) increases activation and expression of endothelia nitric oxide synthase in the cerebrovasculature, an effect associated with a reduction of arteriolar hypertrophy and a delay in the onset of stroke (Xu et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Capsaicin protects cortical neurons against ischemia/reperfusion injury via down-regulating NMDA receptors

Huang

Cheng

Tan

et al. 2017

Experimental Neurology

View full text Add to dashboard Cite

Capsaicin, the ingredient responsible for the pungent taste of hot chili peppers, is widely used in the study and management of pain. Recently, its neuroprotective effect has been described in multiple studies. Herein, we investigated the underlying mechanisms for the neuroprotective effect of capsaicin. Direct injection of capsaicin (1 or 3 nmol) into the peri-infarct area reduced the infarct volume and improved neurological behavioral scoring and motor coordination function in the middle cerebral artery occlusion (MCAO)/reperfusion model in rats. The time window of the protective effect of capsaicin was within 1 h after reperfusion, when excitotoxicity is the main reason of cell death. In cultured cortical neurons, administration of capsaicin attenuated glutamate-induced excitotoxic injury. With respect to the mechanisms of the neuroprotective effect of capsaicin, reduced calcium influx after glutamate stimulation was observed following capsaicin pretreatment in cortical neurons. Trpv1 knockout abolished the inhibitory effect of capsaicin on glutamate-induced calcium influx and subsequent neuronal death. Reduced expression of GluN1 and GluN2B, subunits of NMDA receptor, was examined after capsaicin treatment in cortical neurons. In summary, our studies reveal that the neuroprotective effect of capsaicin in cortical neurons is TRPV1-dependent and down-regulation of the expression and function of NMDA receptors contributes to the protection afforded by capsaicin.

show abstract

“…4 The development of lung I/R injury leads to prolonged duration of mechanical ventilation, increased attendance in intensive care unit, duration of hospital stays and high morbidity and mortality. 6,7 Autophagy is considered as an evolutionary highly conversed process among all eukaryotes ranging from yeast to mammals. 6,7 Autophagy is considered as an evolutionary highly conversed process among all eukaryotes ranging from yeast to mammals.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of mitochondrial autophagy protects donor lungs for lung transplantation against ischaemia‐reperfusion injury in rats via the mTOR pathway

Liu

Chen

Liu

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

Impaired mitochondrial function is a key factor attributing to lung ischaemia‐reperfusion (IR) injury, which contributes to major post‐transplant complications. Thus, the current study was performed to investigate the role of mitochondrial autophagy in lung I/R injury and the involvement of the mTOR pathway. We established rat models of orthotopic left lung transplantation to investigate the role of mitochondrial autophagy in I/R injury following lung transplantation. Next, we treated the donor lungs with 3‐MA and Rapamycin to evaluate mitochondrial autophagy, lung function and cell apoptosis with different time intervals of cold ischaemia preservation and reperfusion. In addition, mitochondrial autophagy, and cell proliferation and apoptosis of pulmonary microvascular endothelial cells (PMVECs) exposed to hypoxia‐reoxygenation (H/R) were monitored after 3‐MA administration or Rapamycin treatment. The cell apoptosis could be inhibited by mitochondrial autophagy at the beginning of lung ischaemia, but was rendered out of control when mitochondrial autophagy reached normal levels. After I/R of donor lung, the mitochondrial autophagy was increased until 6 hours after reperfusion and then gradually decreased. The elevation of mitochondrial autophagy was accompanied by promoted apoptosis, aggravated lung injury and deteriorated lung function. Moreover, the suppression of mitochondrial autophagy by 3‐MA inhibited cell apoptosis of donor lung to alleviate I/R‐induced lung injury as well as inhibited H/R‐induced PMVEC apoptosis, and enhanced its proliferation. Finally, mTOR pathway participated in I/R‐ and H/R‐mediated mitochondrial autophagy in regulation of cell apoptosis. Inhibition of I/R‐induced mitochondrial autophagy alleviated lung injury via the mTOR pathway, suggesting a potential therapeutic strategy for lung I/R injury.

show abstract

TRPV1 Agonist Capsaicin Attenuates Lung Ischemia-Reperfusion Injury in Rabbits

Cited by 40 publications

References 34 publications

Hydrogen-Rich Saline Attenuates Lung Ischemia-Reperfusion Injury in Rabbits

Hydrogen-Rich Saline Attenuates Lung Ischemia-Reperfusion Injury in Rabbits

Capsaicin protects cortical neurons against ischemia/reperfusion injury via down-regulating NMDA receptors

Inhibition of mitochondrial autophagy protects donor lungs for lung transplantation against ischaemia‐reperfusion injury in rats via the mTOR pathway

Contact Info

Product

Resources

About