scholarly journals Renal-Protective Effects and Potential Mechanisms of Traditional Chinese Medicine after Ischemia-Reperfusion Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Demin Liu ◽  
Songling Tang ◽  
Lu Gan ◽  
Wei Cui
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fission ◽  
Hypovolemic Shock ◽  
Kidney Injury ◽  
Protective Effects ◽  
Underlying Mechanisms ◽  
Anti Inflammation

Renal ischemia-reperfusion (I/R) injury mainly causes acute kidney injury (AKI) after renal transplantation, trauma, sepsis, and hypovolemic shock. Patients with renal I/R injury are frequently associated with a poor prognosis. Traditional Chinese medicine (TCM) has been used for the prevention and treatment of various diseases in China and other Asian countries for centuries. Many studies have shown the protective effect of TCM on renal I/R injury, due to its diverse bioactive components. The potential mechanisms of TCMs on renal I/R injury include anti-inflammation, antioxidative effect, anti-cell death, downregulation of adhesion molecule expression, regulation of energy metabolism by restoring Na+-K+-ATPase activity, and mitochondrial fission. This review summarizes the major developments in the effects and underlying mechanisms of TCMs on the renal I/R injury.

Endogenous hydrogen sulphide mediates the cardioprotection induced by ischemic postconditioning

2008 ◽  
Vol 295 (3) ◽  
pp. H1330-H1340 ◽  
Author(s):  
Qian Chen Yong ◽  
Shiau Wei Lee ◽  
Chun Shin Foo ◽  
Kay Li Neo ◽  
Xin Chen ◽  
...  
Keyword(s):  
Hydrogen Sulphide ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Early Period ◽  
Ischemic Postconditioning ◽  
Myocardial Infarct Size ◽  
Protective Effects ◽  
Rat Hearts ◽  
Underlying Mechanisms

The present study aimed to investigate the role of hydrogen sulphide (H2S) in the cardioprotection induced by ischemic postconditioning and to examine the underlying mechanisms. Cardiodynamics and myocardial infarction were measured in isolated rat hearts. Postconditioning with six episodes of 10-s ischemia (IPostC) significantly improved cardiodynamic function, which was attenuated by the blockade of endogenous H2S production with d-l-propargylglycine. Moreover, IPostC significantly stimulated H2S synthesis enzyme activity during the early period of reperfusion. However, d-l-propargylglycine only attenuated the IPostC-induced activation of PKC-α and PKC-ε but not that of PKC-δ, Akt, and endothelial nitric oxide synthase (eNOS). These data suggest that endogenous H2S contributes partially to the cardioprotection of IPostC via stimulating PKC-α and PKC-ε. Postconditioning with six episodes of a 10-s infusion of NaHS (SPostC) or 2 min continuous NaHS infusion (SPostC2) stimulated activities of Akt and PKC, improved the cardiodynamic performances, and reduced myocardial infarct size. The blockade of Akt with LY-294002 (15 μM) or PKC with chelerythrine (10 μM) abolished the cardioprotection induced by H2S postconditioning. SPostC2, but not SPostC, also additionally stimulated eNOS. We conclude that endogenous H2S contributes to IPostC-induced cardioprotection. H2S postconditioning confers the protective effects against ischemia-reperfusion injury through the activation of Akt, PKC, and eNOS pathways.

scholarly journals Ischemia-Reperfusion Injury in Peripheral Artery Disease and Traditional Chinese Medicine Treatment

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Zenghui Liang ◽  
Wentao Zhang ◽  
Tianyi Zhu ◽  
Yunsong Li ◽  
Pengkai Cao ◽  
...  
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Mitochondrial Dysfunction ◽  
Reperfusion Injury ◽  
Peripheral Artery Disease ◽  
Ischemia Reperfusion Injury ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Peripheral Artery ◽  
Artery Disease

Peripheral artery disease (PAD) is a serious public health issue, characterized by circulation disorder of the lower extreme that reduces the physical activity of the lower extremity muscle. The artery narrowed by atherosclerotic lesions initiates limb ischemia. In the progression of treatment, reperfusion injury is still inevitable. Ischemia-reperfusion injury induced by PAD is responsible for hypoxia and nutrient deficiency. PAD triggers hindlimb ischemia and reperfusion (I/R) cycles through various mechanisms, mainly including mitochondrial dysfunction and inflammation. Alternatively, mitochondrial dysfunction plays a central role. The I/R injury may cause cells’ injury and even death. However, the mechanism of I/R injury and the way of cell damage or death are still unclear. We review the pathophysiology of I/R injury, which is majorly about mitochondrial dysfunction. Then, we focus on the cell damage and death during I/R injury. Further comprehension of the progress of I/R will help identify biomarkers for diagnosis and therapeutic targets to PAD. In addition, traditional Chinese medicine has played an important role in the treatment of I/R injury, and we will make a brief introduction.

scholarly journals Antiplatelet Therapy with Integrated Traditional Chinese and Western Medicine for Use in Myocardial Ischemia-Reperfusion Injury: A Review of Clinical Applications and Mechanisms

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Yuxuan Li ◽  
Yan Li ◽  
Bin Li ◽  
Yang Liu ◽  
Jingqian Zhang ◽  
...  
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Antiplatelet Therapy ◽  
Western Medicine ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Myocardial ischemia-reperfusion injury (MIRI) is common in patients with acute coronary syndrome (ACS) after PCI treatment, which seriously affects the efficacy of revascularization and hinders the postoperative recovery of patients; therefore, the current study is focused on determining effective methods in the treatment of MIRI. Antiplatelet therapy is a routine treatment for ACS, and its benefits for treating MIRI have been previously verified. With the development of traditional Chinese medicine (TCM), many TCM preparations are widely used in the clinic. Many basic and clinical studies have shown that TCM can be used together with antiplatelet drugs, and the safety and efficacy when TCM is included in the treatment are better than when antiplatelet drugs are used alone. This paper summarizes the current research progress of traditional Chinese medicine and Western medicine in the treatment of MIRI to provide a theoretical basis for further research and clinical treatment.

scholarly journals C-type lectin Mincle mediates cell death–triggered inflammation in acute kidney injury

2020 ◽  
Vol 217 (11) ◽  
Author(s):  
Miyako Tanaka ◽  
Marie Saka-Tanaka ◽  
Kozue Ochi ◽  
Kumiko Fujieda ◽  
Yuki Sugiura ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cell Death ◽  
Free Cholesterol ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Sterile Inflammation ◽  
Renal Tubular Cell ◽  
Renal Tubules ◽  
Underlying Mechanisms

Accumulating evidence indicates that cell death triggers sterile inflammation and that impaired clearance of dead cells causes nonresolving inflammation; however, the underlying mechanisms are still unclear. Here, we show that macrophage-inducible C-type lectin (Mincle) senses renal tubular cell death to induce sustained inflammation after acute kidney injury in mice. Mincle-deficient mice were protected against tissue damage and subsequent atrophy of the kidney after ischemia–reperfusion injury. Using lipophilic extract from the injured kidney, we identified β-glucosylceramide as an endogenous Mincle ligand. Notably, free cholesterol markedly enhanced the agonistic effect of β-glucosylceramide on Mincle. Moreover, β-glucosylceramide and free cholesterol accumulated in dead renal tubules in proximity to Mincle-expressing macrophages, where Mincle was supposed to inhibit clearance of dead cells and increase proinflammatory cytokine production. This study demonstrates that β-glucosylceramide in combination with free cholesterol acts on Mincle as an endogenous ligand to induce cell death–triggered, sustained inflammation after acute kidney injury.

DPP4 inhibition improves functional outcome after renal ischemia-reperfusion injury

2012 ◽  
Vol 303 (5) ◽  
pp. F681-F688 ◽  
Author(s):  
Lorenzo L. F. Glorie ◽  
Anja Verhulst ◽  
Veerle Matheeussen ◽  
Lesley Baerts ◽  
Joanna Magielse ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Mrna Expression ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Protective Effects ◽  
Dipeptidyl Peptidase 4 ◽  
Dpp4 Inhibition

Dipeptidyl peptidase 4 (DPP4) is an exopeptidase which modulates the function of its substrates, among which are insulin-releasing incretins. DPP4 inhibitors are currently used to improve glucose tolerance in type 2 diabetes patients. Inhibition of DPP4 exhibits protective effects on ischemia-reperfusion injury (IRI) of the heart and lung. As DPP4 and its substrates are also expressed in the kidney, we studied the effect of the DPP4 inhibitor vildagliptin on the outcome of IRI-induced acute kidney injury in rats in a model of 30-min unilateral renal ischemia, followed by contralateral nephrectomy. Saline, 1, or 10 mg/kg vildagliptin (VG1/VG10) was administered intravenously 15 min before the surgery. Animals were euthanized after 2, 12, amd 48 h of reperfusion. DPP4 inhibition resulted in a significant dose-dependent decrease in serum creatinine (1.31 ± 0.32 and 0.70 ± 0.19 mg/dl for VG1 and VG10, respectively, vs. 1.91 ± 0.28 mg/dl for controls at 12 h; P < 0.01). Tubular morphology (PAS-PCNA) revealed significantly reduced tubular necrosis at 12 h (62.1 ± 18.0 and 77.5 ± 22.0% in VG10 and saline, respectively). VG did not affect regeneration but decreased apoptosis, as shown by twofold decreased Bax/Bcl-2 mRNA expression and a threefold decrease in apoptotic bodies on terminal deoxynucleotidyl transferase dUTP nick-end labeling-stained sections. VG treatment significantly reduced serum malondialdehyde twofold in both VG1- and VG10-treated ischemic and sham-operated animals compared with controls and also resulted in a significant decrease in mRNA expression of the proinflammatory marker CXCL10 at 2 h of reperfusion. Through a mechanism yet to be fully understood, VG treatment results in a functional protection of the kidney against IRI. This protection was associated with antiapoptotic, immunological, and antioxidative changes.

scholarly journals The Protective Effect of Traditional Chinese Medicine on Liver Ischemia-Reperfusion Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Wen Ma ◽  
Songling Tang ◽  
Dina Xie ◽  
Guoqiang Gu ◽  
Lu Gan
Keyword(s):  
Endoplasmic Reticulum ◽  
Chinese Medicine ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Traditional Chinese Medicines ◽  
Protective Effects ◽  
Liver Ischemia ◽  
Hepatic Surgery ◽  
Chinese Medicines

Liver ischemia-reperfusion (I/R) injury occurs during transplantation and major hepatic surgery, which may lead to postoperative liver dysfunction. More and more traditional Chinese medicines (TCMs) have been used to treat liver ischemia-reperfusion injury. The purpose of this review is to evaluate the different protective effects of TCMs in the treatment of liver ischemia-reperfusion injury and to summarize its possible mechanisms. The results indicate that TCMs attenuate liver I/R injury via multiple mechanisms, including antioxidation stress, anti-inflammatory response, antiapoptosis, and inhibiting endoplasmic reticulum stress. However, the in-depth mechanism of the protective effects of these traditional Chinese medicines still remains unknown.

scholarly journals Dynamin-Related Protein 1 Deficiency Promotes Recovery from AKI

2017 ◽  
Vol 29 (1) ◽  
pp. 194-206 ◽  
Author(s):  
Heather M. Perry ◽  
Liping Huang ◽  
Rebecca J. Wilson ◽  
Amandeep Bajwa ◽  
Hiromi Sesaki ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Mitochondrial Function ◽  
Ischemia Reperfusion Injury ◽  
Mitochondrial Dynamics ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fission ◽  
Kidney Injury ◽  
Related Protein

The proximal tubule epithelium relies on mitochondrial function for energy, rendering the kidney highly susceptible to ischemic AKI. Dynamin-related protein 1 (DRP1), a mediator of mitochondrial fission, regulates mitochondrial function; however, the cell-specific and temporal role of DRP1 in AKI in vivo is unknown. Using genetic murine models, we found that proximal tubule–specific deletion of Drp1 prevented the renal ischemia-reperfusion–induced kidney injury, inflammation, and programmed cell death observed in wild-type mice and promoted epithelial recovery, which associated with activation of the renoprotective β-hydroxybutyrate signaling pathway. Loss of DRP1 preserved mitochondrial structure and reduced oxidative stress in injured kidneys. Lastly, proximal tubule deletion of DRP1 after ischemia-reperfusion injury attenuated progressive kidney injury and fibrosis. These results implicate DRP1 and mitochondrial dynamics as an important mediator of AKI and progression to fibrosis and suggest that DRP1 may serve as a therapeutic target for AKI.

scholarly journals Targeting Dynamin 2 as a Novel Pathway to Inhibit Cardiomyocyte Apoptosis Following Oxidative Stress

2016 ◽  
Vol 39 (6) ◽  
pp. 2121-2134 ◽  
Author(s):  
Danchen Gao ◽  
Jian Yang ◽  
Yutao Wu ◽  
Qiwen Wang ◽  
Qiaoling Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fission ◽  
Mitochondrial Morphology ◽  
Ros Production ◽  
Protective Effects ◽  
Mitochondrial Fragmentation ◽  
Induced Apoptosis ◽  
Dynamin 2

Background/Aims: Inhibition of Drp-1-mediated mitochondrial fission limits reactive oxygen species (ROS) production and apoptosis in cardiomyocytes subjected to ischemia/reperfusion injury. It remains unknown if Dynamin 2 inhibition results in similar protective effects. Here we studied the role of Dynamin 2 in cardiomyocyte oxidative stress-induced apoptosis and ROS production. Methods: The effect of lentiviral shRNA (lv5-shRNA) mediated Dynamin 2 knockdown on apopotosis, mitochondria, and ROS production were studied in neonatal mouse cardiomycytes, which were further treated with either selective Drp1 inhibitor mdivi-1 or the Dynamin 2/Drp1 inhibitor Dynasore. Apoptosis was evaluated by flow cytometry. Mitochondrial morphology and transmembrane potential (ΔΨm) were studied by confocal microscopy, and ROS production was detected by dichlorofluorescein diacetate. Results: Inhibition of Drp1 and Dynamin 2 protected against mitochondrial fragmentation, maintained ΔΨm, attenuated cellular ROS production and limited apoptosis. Moreover, Lv5-shRNA mediated knockdown of Dynamin 2 alleviated mitochondrial fragmentation, and reduced both ROS production and oxidative stress-induced apoptosis. The protective effects of Dynamin 2 knockdown were enhanced by Dynasore, indicating an added benefit. Conclusions: Oxidative stress-induced apoptosis and ROS production are attenuated by not only Drp1 inhibition but also Dynamin 2 inhibition, implicating Dynamin 2 as a mediator of oxidative stress in cardiomyocytes.

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