Hui Chen1, Bianzhi Xing2, Lei Wang3, Xiaodong Weng3, Zhiyuan Chen3, Xiuheng Liu3. 1. Department of Urology, Renmin Hospital of Wuhan University, Wuhan, China. Electronic address: drchenhuiyx@163.com. 2. Department of Radiology, Renmin Hospital of Wuhan University, Wuhan, China. 3. Department of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Abstract
OBJECTIVE: To investigate whether the protective effects of ischemic postconditioning (IPoC) are associated with the modulation of toll-like receptor 4 (TLR4) expression. METHODS: We subjected Wistar rats to 45 minutes of ischemia followed by reperfusion at 24 hours. Before reperfusion, rats were treated with 6 cycles of 10 seconds of reperfusion followed by 10 seconds of ischemia. Blood samples were collected for the detection of blood urea nitrogen and creatinine levels. Histologic examinations were evaluated, and immunohistochemistry was also performed for localization of TLR4. The expression of TNF-α, IL-1β, IL-6, MCP-1, and TLR4 were studied by real-time polymerase chain reaction or Western blot. RESULTS: The results indicated that blood urea nitrogen and creatinine levels increased significantly in the ischemia/reperfusion (I/R) group. Rats treated with IPoC showed obviously less renal damage. Immunohistochemistry showed that TLR4 was ameliorated by IPoC. Real-time polymerase chain reaction showed that IPoC could significantly inhibit the increased messenger ribonucleic acid level of TNF-α, IL-1β, IL-6, MCP-1, and TLR4 induced by I/R. Western blot indicated that the expression of TLR4 was upregulated in I/R group, but IPoC could inhibit this increase. CONCLUSION: These findings indicated that IPoC could reduce the expression of TLR4 after renal I/R injury, and the modulation of TLR4 may play a role in the renoprotective effect of IPoC.
OBJECTIVE: To investigate whether the protective effects of ischemic postconditioning (IPoC) are associated with the modulation of toll-like receptor 4 (TLR4) expression. METHODS: We subjected Wistar rats to 45 minutes of ischemia followed by reperfusion at 24 hours. Before reperfusion, rats were treated with 6 cycles of 10 seconds of reperfusion followed by 10 seconds of ischemia. Blood samples were collected for the detection of blood ureanitrogen and creatinine levels. Histologic examinations were evaluated, and immunohistochemistry was also performed for localization of TLR4. The expression of TNF-α, IL-1β, IL-6, MCP-1, and TLR4 were studied by real-time polymerase chain reaction or Western blot. RESULTS: The results indicated that blood ureanitrogen and creatinine levels increased significantly in the ischemia/reperfusion (I/R) group. Rats treated with IPoC showed obviously less renal damage. Immunohistochemistry showed that TLR4 was ameliorated by IPoC. Real-time polymerase chain reaction showed that IPoC could significantly inhibit the increased messenger ribonucleic acid level of TNF-α, IL-1β, IL-6, MCP-1, and TLR4 induced by I/R. Western blot indicated that the expression of TLR4 was upregulated in I/R group, but IPoC could inhibit this increase. CONCLUSION: These findings indicated that IPoC could reduce the expression of TLR4 after renal I/R injury, and the modulation of TLR4 may play a role in the renoprotective effect of IPoC.
Authors: Simone J Jonker; Theo P Menting; Michiel C Warlé; Merel Ritskes-Hoitinga; Kimberley E Wever Journal: PLoS One Date: 2016-03-10 Impact factor: 3.240