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 ◽  
...  

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.

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Yuxuan Li ◽  
Yan Li ◽  
Bin Li ◽  
Yang Liu ◽  
Jingqian Zhang ◽  
...  

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.


2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Jiheng Zhan ◽  
Xing Li ◽  
Dan Luo ◽  
Wanying Yan ◽  
Yonghui Hou ◽  
...  

Spinal cord ischemia/reperfusion injury (SCII) is a devastating complication of spinal or thoracic surgical procedures and can lead to paraplegia or quadriplegia. Neuronal cell damage involving mitochondrial dysfunction plays an important role in the pathogenesis of SCII. Despite the availability of various treatment options, there are currently no mitochondria-targeting drugs that have proven effective against SCII. Polydatin (PD), a glucoside of resveratrol, is known to preserve mitochondrial function in central nervous system (CNS) diseases. The aim of the present study was to explore the neuro- and mito-protective functions of PD and its underlying mechanisms. An in vitro model of SCII was established by exposing spinal cord motor neurons (SMNs) to oxygen–glucose-deprivation/reperfusion (OGD/R), and the cells were treated with different dosages of PD for varying durations. PD improved neuronal viability and protected against OGD/R-induced apoptosis and mitochondrial injury in a dose-dependent manner. In addition, PD restored the activity of neuronal mitochondria in terms of mitochondrial membrane potential (MMP), intracellular calcium levels, mitochondrial permeability transition pore (mPTP) opening, generation of reactive oxygen species (ROS), and adenosine triphosphate (ATP) levels. Mechanistically, PD downregulated Keap1 and upregulated Nrf2, NQO-1, and HO-1 in the OGD/R-treated SMNs. Likewise, PD treatment also reversed the neuronal and mitochondrial damage induced by SCII in a mouse model. Furthermore, the protective effects of PD were partially blocked by the Nrf2 inhibitor. Taken together, PD relieves mitochondrial dysfunction-induced neuronal cell damage by activating the Nrf2/ARE pathway and is a suitable therapeutic option for SCII.


2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Hehe Cui ◽  
Xiangdong Li ◽  
Zhigang Wang ◽  
Na Li ◽  
Kang Qi ◽  
...  

Cardiac microvascular endothelial cells (CMECs) regulate the function of cardiomyocytes and blood cells in myocardial ischemia/ reperfusion injury (MIRI) via paracrine methods. Tongxinluo (TXL) is a Traditional Chinese Medicine compound to treat angina pectoris in China, which is constituted of ginseng and other 11 natural products. It is proved to improve the endothelial function and be protective against MIRI. Thus, we aimed to find alterations in paracrine function of CMECs under the hypoxia/reoxygenation (H/R) situation and its modulation by TXL. CMECs were exposed to different concentrations of TXL for 30 min and then subjected to H/R for 12 h/2 h. Apoptotic rates were measured to determine the optimal concentration. Protein antibody arrays were used to find the alterations of cytokines in conditioned medium (CM) secreted by CMECs. Gene Ontology project was adopted to describe the functions of changed cytokines. TXL inhibited apoptosis of CMECs dose-dependently under H/R and reached its peak effect at 800 μg/mL. Thirty-three types of cytokines were significantly changed by H/R (19 factors decreased and 14 increased), and TXL at 800μg/ml changed 121 types of cytokines compared to the H/R group (93 factors decreased and 28 increased). The cytokines with significant alterations were involved in cell differentiation and proliferation, positive chemotaxis, and endothelial cell migration. Among these cytokines, bFGF, PDGF and IL-7 were attenuated by H/R and further decreased by TXL, while IL-21, MCP-2 and GROa were increased by H/R but decreased by TXL. The study elucidated the paracrine function of CMECs in MIRI and partly illuminated the protective mechanisms of TXL.


2020 ◽  
Author(s):  
Yan Zhang ◽  
Yao Lu ◽  
Kai Wang ◽  
Mei-yan Zhou ◽  
Cong-you Wu ◽  
...  

Abstract Background: Lung ischemia-reperfusion injury (LIRI) is a significant clinical problem occurring after lung transplantation. LIRI is mediated by the overproduction of reactive oxygen species (ROS) and inflammatory activation. Previous studies have confirmed that dexmedetomidine (DEX) exerts a protective effect on LIRI, which potentially causes severe mitochondrial dysfunction. However, the specific mechanisms remain unclear. Our study was to explore whether dexmedetomidine exerts a beneficial effect on LIRI by reducing mitochondrial dysfunction. Methods: Two different models were used in our study. For the in vivo experiment, thirty-two male Sprague-Dawley rats were randomly divided into Sham, ischemia-reperfusion (I/R), DEX+I/R and DEX+yohimbine+I/R (DY+I/R) groups. Similarly, pulmonary vascular endothelial cells (PVECs) from SD rats were divided into Control, oxygen glucose deprivation (OGD), D+OGD and DY+OGD groups.Results: In our experiment, we confirmed severe lung damage after LIRI that was characterized by significantly pulmonary histopathology injury, a decrease in the oxygenation index (PaO2/FiO2) and an increase in the wet-to-dry weight ratio, while DEX treatment mitigated this damage. In addition, the DEX pretreatment significantly attenuated I/R-induced oxidative stress by decreasing the level of ROS in the mitochondria in vitro. Moreover, the DEX treatment enhanced mitochondrial biogenesis and autophagy by increasing the expression of peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α), mitochondrial transcription factor A (Tfam), PTEN-induced putative kinase 1 (PINK1), Parkin and dynamin 1-like protein 1 (Drp1). Conclusions: These data suggest that DEX may alleviate LIRI by reducing mitochondrial dysfunction through the induction of mitochondrial biogenesis and autophagy.


2015 ◽  
Vol 10 (5) ◽  
pp. 415-429 ◽  
Author(s):  
Giuseppe Paradies ◽  
Valeria Paradies ◽  
Francesca M Ruggiero ◽  
Giuseppe Petrosillo

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