The Experts below are selected from a list of 4203 Experts worldwide ranked by ideXlab platform
Zhiyuan Chen - One of the best experts on this subject based on the ideXlab platform.
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Ischemic Postconditioning inhibits apoptosis of renal cells following reperfusion: a novel in vitro model.
International Urology and Nephrology, 2015Co-Authors: Xiaodong Weng, Hui Chen, Zhiyuan Chen, Min Wang, Xiuheng LiuAbstract:Purpose The majority of renal Ischemic/reperfusion (I/R) and Ischemic Postconditioning (IPO) studies have been based on animal models. To gain mechanistic insights into Ischemic Postconditioning-induced alterations at the cell level, a novel in vitro model of I/R and IPO is set up by using the rat proximal tubule cell line NRK-52E.
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Ischemic Postconditioning inhibits the renal fibrosis induced by ischemia-reperfusion injury in rats.
Urology, 2012Co-Authors: Xiaodong Weng, Zhiyuan Chen, Hao Shen, You-lin Kuang, Xiuhen Liu, Henchen Zhu, Bo-tao Jiang, Guohui Zhu, Hui ChenAbstract:Objective To investigate whether Ischemic Postconditioning effects on the development of tubulointerstitial fibrosis follow acute renal ischemia-reperfusion. Methods Rat models of warm renal I/R were established by clamping left pedicles for 45 minutes after right nephrectomy, both with and without treatment with Ischemic Postconditioning, and then reperfused for up to 12 weeks. Hematoxylin–eosin (H&E) and Masson's trichrome staining were used to assess renal fibrosis. The expression spot and protein levels of α-smooth muscle actin (α-SMA), transforming growth factor–β1 (TGF-β1), and phospho-Smad2 were also analyzed. Results Our data showed that patchy inflammation and tubulointerstitial fibrosis were found 12 weeks later in rats subjected to I/R alone or with Postconditioning. Tubulointerstitial fibrosis worsened further in rats subjected to 45-minute ischemia-reperfusion, accompanied by the increased expressions of α-SMA, TGF-β1, and phospho-Smad2 at the end of 12 weeks. In contrast, the above histologic changes and molecular expressions were significantly attenuated in rats of Ischemic Postconditioning group. Conclusion The results indicated that 45-minute I/R injury may cause tubulointerstitial fibrosis in the long term, and Ischemic Postconditioning has beneficial effects on renal fibrosis. Its mechanisms may involve inhibition of the TGF-β1/phospho-Smad2 pathway to exert protective effects.
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Ischemic Postconditioning inhibits apoptosis after renal ischemia reperfusion injury in rat
Transplant International, 2008Co-Authors: Hui Chen, Bianzhi Xing, Xiuheng Liu, Bingyan Zhan, Jiangqiao Zhou, Heng-cheng Zhu, Zhiyuan ChenAbstract:Summary Ischemic Postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of Ischemic Postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with Ischemic Postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that Ischemic Postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that Ischemic Postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
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Ischemic Postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat.
Transplant International, 2008Co-Authors: Hui Chen, Bianzhi Xing, Xiuheng Liu, Bingyan Zhan, Jiangqiao Zhou, Heng-cheng Zhu, Zhiyuan ChenAbstract:Summary Ischemic Postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of Ischemic Postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with Ischemic Postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that Ischemic Postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that Ischemic Postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
Hui Chen - One of the best experts on this subject based on the ideXlab platform.
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Ischemic Postconditioning inhibits apoptosis of renal cells following reperfusion: a novel in vitro model.
International Urology and Nephrology, 2015Co-Authors: Xiaodong Weng, Hui Chen, Zhiyuan Chen, Min Wang, Xiuheng LiuAbstract:Purpose The majority of renal Ischemic/reperfusion (I/R) and Ischemic Postconditioning (IPO) studies have been based on animal models. To gain mechanistic insights into Ischemic Postconditioning-induced alterations at the cell level, a novel in vitro model of I/R and IPO is set up by using the rat proximal tubule cell line NRK-52E.
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Ischemic Postconditioning inhibits the renal fibrosis induced by ischemia-reperfusion injury in rats.
Urology, 2012Co-Authors: Xiaodong Weng, Zhiyuan Chen, Hao Shen, You-lin Kuang, Xiuhen Liu, Henchen Zhu, Bo-tao Jiang, Guohui Zhu, Hui ChenAbstract:Objective To investigate whether Ischemic Postconditioning effects on the development of tubulointerstitial fibrosis follow acute renal ischemia-reperfusion. Methods Rat models of warm renal I/R were established by clamping left pedicles for 45 minutes after right nephrectomy, both with and without treatment with Ischemic Postconditioning, and then reperfused for up to 12 weeks. Hematoxylin–eosin (H&E) and Masson's trichrome staining were used to assess renal fibrosis. The expression spot and protein levels of α-smooth muscle actin (α-SMA), transforming growth factor–β1 (TGF-β1), and phospho-Smad2 were also analyzed. Results Our data showed that patchy inflammation and tubulointerstitial fibrosis were found 12 weeks later in rats subjected to I/R alone or with Postconditioning. Tubulointerstitial fibrosis worsened further in rats subjected to 45-minute ischemia-reperfusion, accompanied by the increased expressions of α-SMA, TGF-β1, and phospho-Smad2 at the end of 12 weeks. In contrast, the above histologic changes and molecular expressions were significantly attenuated in rats of Ischemic Postconditioning group. Conclusion The results indicated that 45-minute I/R injury may cause tubulointerstitial fibrosis in the long term, and Ischemic Postconditioning has beneficial effects on renal fibrosis. Its mechanisms may involve inhibition of the TGF-β1/phospho-Smad2 pathway to exert protective effects.
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Ischemic Postconditioning inhibits apoptosis after renal ischemia reperfusion injury in rat
Transplant International, 2008Co-Authors: Hui Chen, Bianzhi Xing, Xiuheng Liu, Bingyan Zhan, Jiangqiao Zhou, Heng-cheng Zhu, Zhiyuan ChenAbstract:Summary Ischemic Postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of Ischemic Postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with Ischemic Postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that Ischemic Postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that Ischemic Postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
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Ischemic Postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat.
Transplant International, 2008Co-Authors: Hui Chen, Bianzhi Xing, Xiuheng Liu, Bingyan Zhan, Jiangqiao Zhou, Heng-cheng Zhu, Zhiyuan ChenAbstract:Summary Ischemic Postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of Ischemic Postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with Ischemic Postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that Ischemic Postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that Ischemic Postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
Xiuheng Liu - One of the best experts on this subject based on the ideXlab platform.
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Ischemic Postconditioning inhibits apoptosis of renal cells following reperfusion: a novel in vitro model.
International Urology and Nephrology, 2015Co-Authors: Xiaodong Weng, Hui Chen, Zhiyuan Chen, Min Wang, Xiuheng LiuAbstract:Purpose The majority of renal Ischemic/reperfusion (I/R) and Ischemic Postconditioning (IPO) studies have been based on animal models. To gain mechanistic insights into Ischemic Postconditioning-induced alterations at the cell level, a novel in vitro model of I/R and IPO is set up by using the rat proximal tubule cell line NRK-52E.
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Ischemic Postconditioning inhibits apoptosis after renal ischemia reperfusion injury in rat
Transplant International, 2008Co-Authors: Hui Chen, Bianzhi Xing, Xiuheng Liu, Bingyan Zhan, Jiangqiao Zhou, Heng-cheng Zhu, Zhiyuan ChenAbstract:Summary Ischemic Postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of Ischemic Postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with Ischemic Postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that Ischemic Postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that Ischemic Postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
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Ischemic Postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat.
Transplant International, 2008Co-Authors: Hui Chen, Bianzhi Xing, Xiuheng Liu, Bingyan Zhan, Jiangqiao Zhou, Heng-cheng Zhu, Zhiyuan ChenAbstract:Summary Ischemic Postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of Ischemic Postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with Ischemic Postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that Ischemic Postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that Ischemic Postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
Heng-cheng Zhu - One of the best experts on this subject based on the ideXlab platform.
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Ischemic Postconditioning inhibits apoptosis after renal ischemia reperfusion injury in rat
Transplant International, 2008Co-Authors: Hui Chen, Bianzhi Xing, Xiuheng Liu, Bingyan Zhan, Jiangqiao Zhou, Heng-cheng Zhu, Zhiyuan ChenAbstract:Summary Ischemic Postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of Ischemic Postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with Ischemic Postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that Ischemic Postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that Ischemic Postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
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Ischemic Postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat.
Transplant International, 2008Co-Authors: Hui Chen, Bianzhi Xing, Xiuheng Liu, Bingyan Zhan, Jiangqiao Zhou, Heng-cheng Zhu, Zhiyuan ChenAbstract:Summary Ischemic Postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of Ischemic Postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with Ischemic Postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that Ischemic Postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that Ischemic Postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
Jiangqiao Zhou - One of the best experts on this subject based on the ideXlab platform.
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Ischemic Postconditioning inhibits apoptosis after renal ischemia reperfusion injury in rat
Transplant International, 2008Co-Authors: Hui Chen, Bianzhi Xing, Xiuheng Liu, Bingyan Zhan, Jiangqiao Zhou, Heng-cheng Zhu, Zhiyuan ChenAbstract:Summary Ischemic Postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of Ischemic Postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with Ischemic Postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that Ischemic Postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that Ischemic Postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
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Ischemic Postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat.
Transplant International, 2008Co-Authors: Hui Chen, Bianzhi Xing, Xiuheng Liu, Bingyan Zhan, Jiangqiao Zhou, Heng-cheng Zhu, Zhiyuan ChenAbstract:Summary Ischemic Postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of Ischemic Postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with Ischemic Postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that Ischemic Postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that Ischemic Postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
