Acute kidney injury (AKI) is an important factor for the occurrence and development of CKD. The protective effect of dihydroartemisinin on AKI and and reported mechanism have not been reported. In this study, we used two animal models including ischemia-reperfusion and UUO, as well as a high-glucose-stimulated HK-2 cell model, to evaluate the protective effect of dihydroartemisinin on premature senescence of renal tubular epithelial cells in vitro and in vivo. We demonstrated that dihydroartemisinin improved renal aging and renal injury by activating autophagy. In addition, we found that co-treatment with chloroquine, an autophagy inhibitor, abolished the anti-renal aging effect of dihydroartemisinin in vitro. These findings suggested that activation of autophagy/elimination of senescent cell might be a useful strategy to prevent AKI/UUO induced renal tubular senescence and fibrosis.
Animals ; Kidney ; Acute Kidney Injury/chemically induced* ; Ischemia ; Reperfusion Injury/drug therapy* ; Autophagy ; Reperfusion

Dexamethasone ; therapeutic use ; Humans ; Liver Diseases ; drug therapy ; Reperfusion Injury ; drug therapy

Methane is the simplest hydrocarbon, consisting of one carbon atom and four hydrogen atoms. It is abundant in marsh gas, livestock rumination, and combustible ice. Little is known about the use of methane in human disease treatment. Current research indicates that methane is useful for treating several diseases including ischemia and reperfusion injury, and inflammatory diseases. The mechanisms underlying the protective effects of methane appear primarily to involve anti-oxidation, anti-inflammation, and anti-apoptosis. In this review, we describe the beneficial effects of methane on different diseases, summarize possible mechanisms by which methane may act in these conditions, and discuss the purpose of methane production in hypoxic conditions. Then we propose several promising directions for the future research.
Antioxidants/pharmacology* ; Apoptosis/drug effects* ; Humans ; Inflammation/drug therapy* ; Ischemia/drug therapy* ; Methane/therapeutic use* ; Reperfusion Injury/drug therapy*

This study aims to explore the effect of Xiaoxuming Decoction on synaptic plasticity in rats with acute cerebral ischemia-reperfusion. A rat model of cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion(MCAO). Rats were randomly assigned into a sham group, a MCAO group, and a Xiaoxuming Decoction(60 g·kg~(-1)·d~(-1)) group. The Longa score was rated to assess the neurological function of rats with cerebral ischemia for 1.5 h and reperfusion for 24 h. The 2,3,5-triphenyltetrazolium chloride(TTC) staining and hematoxylin-eosin(HE) staining were employed to observe the cerebral infarction and the pathological changes of brain tissue after cerebral ischemia, respectively. Transmission electron microscopy was employed to detect the structural changes of neurons and synapses in the ischemic penumbra, and immunofluorescence, Western blot to determine the expression of synaptophysin(SYN), neuronal nuclei(NEUN), and postsynaptic density 95(PSD95) in the ischemic penumbra. The experimental results showed that the modeling increased the Longa score and led to cerebral infarction after 24 h of ischemia-reperfusion. Compared with the model group, Xiaoxuming Decoction intervention significantly decreased the Longa score and reduced the formation of cerebral infarction area. The modeling led to the shrinking and vacuolar changes of nuclei in the brain tissue, disordered cell arrangement, and severe cortical ischemia-reperfusion injury, while the pathological damage in the Xiaoxuming Decoction group was mild. The modeling blurred the synaptic boundaries and broadened the synaptic gap, while such changes were recovered in the Xiaoxuming Decoction group. The modeling decreased the fluorescence intensity of NEUN and SYN, while the intensity in Xiaoxuming Decoction group was significantly higher than that in the model group. The expression of SYN and PSD95 in the ischemic penumbra was down-regulated in the model group, while such down-regulation can be alleviated by Xiaoxuming Decoction. In summary, Xiaoxuming Decoction may improve the synaptic plasticity of ischemic penumbra during acute cerebral ischemia-reperfusion by up-regulating the expression of SYN and PSD95.
Rats ; Animals ; Rats, Sprague-Dawley ; Brain Ischemia/drug therapy* ; Reperfusion Injury/metabolism* ; Infarction, Middle Cerebral Artery ; Neuronal Plasticity ; Reperfusion

Animals ; Codonopsis ; chemistry ; Drugs, Chinese Herbal ; pharmacology ; Myocardial Reperfusion Injury ; drug therapy ; Rats ; Selenium ; pharmacology

Renal ischemia-reperfusion injury (IRI) is histologically characterized by tubular cell death. Diverse pathways of regulated cell death (RCD) have been reported to contribute to renal IRI in recent studies. In this review, we discuss the signaling pathways, regulators and crosstalk of RCD, including necroptosis, ferroptosis and pyroptosis, and their role in renal IRI in order to pave the way for new therapeutic opportunities.
Apoptosis ; Ferroptosis ; Humans ; Kidney/metabolism* ; Necroptosis ; Regulated Cell Death ; Reperfusion Injury/drug therapy*

Animals ; Apoptosis ; Bridged Bicyclo Compounds, Heterocyclic/pharmacology* ; Cell Line ; Hypoxia ; MicroRNAs/genetics* ; Myocardial Reperfusion Injury/drug therapy* ; Myocytes, Cardiac ; Oxidative Stress ; Rats ; Reperfusion Injury ; Tetrahydronaphthalenes/pharmacology*

Reperfusion is the most effective treatment for acute myocardial infarction, markedly reducing mortality and morbidity. Reperfusion however induces necrotic and apoptotic damages to cardiomyocytes, that were viable prior to reperfusion, a process called myocardial ischemia/reperfusion injury(MI/RI). Over the past 30 years, hundreds of experimental interventions (both pharmacologic and nonpharmacologic) have been reported to protect the ischemic myocardium in experimental animals; however, with the exception of early reperfusion, none has been translated into clinical practice. The population-based survey assessed men have about twice the total incidence of morbidity and mortality of women, and the sex gap in morbidity tends to diminish after age 45 years. So hormone replacement therapy (HRT) is given to treat the MI/RI, and lots of studies shows that the side effect is greater for estrogen, compared with phyestrogen. In this article, we review the important pathogenesis of myocardial ischemia reperfusion injury, the prevention and limitations of HRT. And we highlight the mechanism of phyestrogens treatment the MI/RI in experiment. The aim is to provide the theoretically new way of develop the safe and effective products for the researchers.
Animals ; Humans ; Myocardial Ischemia ; drug therapy ; Myocardial Reperfusion Injury ; drug therapy ; Phytoestrogens ; administration & dosage ; Plant Extracts ; administration & dosage

Phosphodiesterase type 5 (PDE5) inhibitors are used most commonly in the treatment of penile erectile dysfunction (ED). Recent studies show that PDE5 inhibitors are ideal drugs for treating ischemia-reperfusion injury. This review focuses on the results of basic and clinical researches on PDE5 inhibitors for the treatment of ischemia-reperfusion injury and provides some theoretical evidence for clinical options of the drugs.
Erectile Dysfunction ; drug therapy ; Humans ; Male ; Phosphodiesterase 5 Inhibitors ; therapeutic use ; Phosphodiesterase Inhibitors ; therapeutic use ; Reperfusion Injury ; drug therapy

OBJECTIVETo investigate the effect of ulinastatin on renal function and ultrastructure changes after renal ischemia-reperfusion in rats.

METHODSAcute ischemic renal injury model was established (45 min of bilateral renal ischemia and reperfusion for 24 h). Thirty Male SD rats were randomly divided into 3 groups: sham operation group (control group or group C, without renal ischemia), renal ischemia-reperfusion group (ischemia-reperfusion group or group I, without ulinastatin), renal ischemia-reperfusion and ulinastatin intravenous injection group (ulinastatin group or group U). BUN level, serum creatinine values and renal ultrastructure were measured.

RESULTSSerum creatinine (167 +/- 39) micromol/L and BUN concentration (21 +/- 7) mmol/L in group I were significantly higher than those in group U: serum creatinine (116 +/- 13) micromol/L and BUN concentration (14.1 +/- 2.6) mmol/L (P < 0.05). The renal ultrastructure was greatly injured in group I, meanwhile, it was obviously ameliorated in group U.

CONCLUSIONUlinastatin greatly improved renal function and provides remarkable protection on renal ultrastructure after ischemia-reperfusion of kidney in rats.

Animals ; Glycoproteins ; pharmacology ; Kidney ; blood supply ; drug effects ; ultrastructure ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; drug therapy ; pathology