NK Cell Regulatory Property is Involved in the Protective Role of MSC-Derived Extracellular Vesicles in Renal Ischemic Reperfusion Injury

2016 ◽  
Vol 27 (11) ◽  
pp. 926-935 ◽  
Author(s):  
Xiangyu Zou ◽  
Di Gu ◽  
Guangyuan Zhang ◽  
Liang Zhong ◽  
Zhongliang Cheng ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Extracellular Vesicles ◽  
Nk Cell ◽  
Protective Role ◽  
Ischemic Reperfusion Injury ◽  
Regulatory Property ◽  
Ischemic Reperfusion ◽  
Renal Ischemic Reperfusion Injury

scholarly journals Role of IL-1 in renal ischemic reperfusion injury.

1998 ◽  
Vol 9 (4) ◽  
pp. 614-619 ◽  
Author(s):  
M Haq ◽  
J Norman ◽  
S R Saba ◽  
G Ramirez ◽  
H Rabb
Keyword(s):  
Renal Function ◽  
Reperfusion Injury ◽  
Interleukin 1 ◽  
Organ Injury ◽  
Central Component ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
And Control ◽  
Renal Ischemic Reperfusion Injury

Interleukin-1 (IL-1) is a central component of many acute inflammatory processes. Blocking IL-1 receptor (IL-1R) with IL-1R antagonist (IL-1Ra) has attenuated ischemic reperfusion injury in brain, heart, and liver models. However, the role of IL-1 in renal ischemic reperfusion injury (IRI) is not known. Therefore, the role of IL-1 in renal IRI was evaluated using the complementary approaches of IL-1R blockade in wild-type mice in addition to the study of renal IRI in IL-1R knockout (KO) mice. Ischemia was induced by bilateral renal pedicle clamping for 30 min. IL-1Ra was administered at 10 mg/kg every 4 h, high doses that have been protective in previous organ injury models in mice. IL-1R KO animals, previously characterized as insensitive to IL-1, had the absence of IL-1R1 confirmed by DNA blots. IL-1Ra, IL-1R KO, and control groups had similar elevations of blood urea nitrogen (114 +/- 13, 133 +/- 11, and 120 +/- 11 mg/dl) and serum creatinine (1.7 +/- 0.3, 2.1 +/- 0.2, and 1.6 +/- 0.3 mg/dl) 24 h after ischemia. Furthermore, acute tubular necrosis scores were also similar in IL-1Ra-treated mice (3.0 +/- 0.3), IL-1R KO mice (2.7 +/- 0.3), and control mice (3.1 +/- 0.2). However, both IL-1Ra and IL-1R KO groups, compared with control animals, developed significantly less infiltration of polymorphonuclear leukocytes per 10 high-power fields in postischemic renal tissue (1111 +/- 228 and 967 +/- 198 versus 1820 +/- 190, P < 0.05). In contrast to the comparable renal functions at 24 h, recovery of renal function was significantly accelerated in the IL-1R KO group compared with control at both 48 (P < 0.05) and 72 (P < 0.05) h. Recovery in the IL-1Ra group was similar to that in the control animals. These data demonstrate that IL-1 is unlikely to be beneficial in the recovery of renal function after ischemia and may play a deleterious role.

Protective role of PEG conjugated phospholipid in reducing ischemic reperfusion injury in two allogeneic pig kidney transplant models

Immunobiology ◽  
2016 ◽  
Vol 221 (10) ◽  
pp. 1184
Author(s):  
Kristina N. Ekdahl ◽  
Yuji Teramura ◽  
Sana Asif ◽  
Elin Manell ◽  
Alireza Biglarnia ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Kidney Transplant ◽  
Protective Role ◽  
Ischemic Reperfusion Injury ◽  
Pig Kidney ◽  
Ischemic Reperfusion

scholarly journals Protective Role of Ramipril and Candesartan against Myocardial Ischemic Reperfusion Injury: A Biochemical and Transmission Electron Microscopical Study

2016 ◽  
Vol 2016 ◽  
pp. 1-7
Author(s):  
Mohamed Saleem Thattakudian Sheik Uduman ◽  
Rajitha Bodd Reddy ◽  
Priyanka Punuru ◽  
Gopinath Chakka ◽  
Gauthaman Karunakaran
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Protective Role ◽  
Global Ischemia ◽  
Protective Mechanism ◽  
Myocardial Tissue ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Transmission Electron

The present study was designed to investigate the role of combined administration of Ramipril and Candesartan againstin vitromyocardial ischemic reperfusion injury in rat. Male Wistar albino rats were divided into five groups (n=6) and treated with saline (10 mL/kg), Ramipril (2 mg/kg), Candesartan (1 mg/kg), and the combination of both drugs, respectively 24 h before induction of global ischemia (5 min of stabilization, 9 min of global ischemia, and 12 min of reflow). Combination of Ramipril and Candesartan when compared to the monotherapy significantly increased the levels of superoxide dismutase, reduced glutathione, catalase, and nitric oxide and decreased the levels of thiobarbituric acid reactive substances. In addition, the superior protective role of combination of Ramipril and Candesartan on ischemia induced myocardial damage was further confirmed by well preserved myocardial tissue architecture in light microscopy and transmission electron microscopy analysis studies. The combination was proved to be effective in salvaging the myocardial tissue against ischemic reperfusion injury when compared to the monotherapy of individual drugs and further investigations on protective mechanism of drugs by increasing the nitric oxide level at molecular levels are needed.

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