Chunyan Zhang1, Yuxia Wang2, Jin Jin2, Kezhong Li3. 1. Department of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Shandong, 264000, PR China; Department of Anesthesiology, School of Medicine, Shandong University, Jinan, Shandong, 250000, PR China. 2. Department of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Shandong, 264000, PR China. 3. Department of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Shandong, 264000, PR China. Electronic address: lunnen7053448@126.com.
Abstract
OBJECTIVE: To explore the protective effect of erythropoietin on propofol induced neuronal injury in developing rats by regulating TLR4/NF-κB signaling pathway. METHOD: Rats were divided into normal control group (Control), propofol group (PPF), erythropoietin group (EPO), propofol + erythropoietin group (P + E), propofol + TAK-242 group (P + T), and propofol + EPO + LPS group (P + E+L) (n = 12). The pathology of hippocampal neurons was observed. The inflammatory factors were detected by ELISA. The expression of TLR4/NF-κB pathway-related proteins were detected by Western blot. RESULTS: Compared with the PPF group, the percentage of apoptotic cells in the hippocampal CA1 area of the erythropoietin treatment groups were greatly decreased while the percentage of positive cells in the hippocampus were remarkably increased(p < 0.05). The production of inflammatory factors and the expressions of TLR4/NF-κB pathway-related proteins were greatly improved in treatment groups (p < 0.05). Compared with P + E group, the percentage of apoptotic cells in CA1 area of the P + E+L group was significantly increased and the percentage of positive cells was remarkably reduced(p < 0.05), the levels of interleukin-1β(IL-1β), interleukin-6(IL-6), interleukin-8(IL-8) and tumor necrosis factor-α(TNF-α) were significantly increased and interleukin-4(IL-4) and interleukin-10(IL-10) was notably reduced(p < 0.05). The protein expression of TLR4 and p-P65 was significantly increased, while the protein expression of p-IκBαwas significantly decreased (p < 0.05). CONCLUSION: Erythropoietin has a protective effect on propofol induced neuropathic injury propofol in rats, and its mechanism is relevant to the regulation of TLR4/NF-κB signaling pathway.
OBJECTIVE: To explore the protective effect of erythropoietin on propofol induced neuronal injury in developing rats by regulating TLR4/NF-κB signaling pathway. METHOD:Rats were divided into normal control group (Control), propofol group (PPF), erythropoietin group (EPO), propofol + erythropoietin group (P + E), propofol + TAK-242 group (P + T), and propofol + EPO + LPS group (P + E+L) (n = 12). The pathology of hippocampal neurons was observed. The inflammatory factors were detected by ELISA. The expression of TLR4/NF-κB pathway-related proteins were detected by Western blot. RESULTS: Compared with the PPF group, the percentage of apoptotic cells in the hippocampal CA1 area of the erythropoietin treatment groups were greatly decreased while the percentage of positive cells in the hippocampus were remarkably increased(p < 0.05). The production of inflammatory factors and the expressions of TLR4/NF-κB pathway-related proteins were greatly improved in treatment groups (p < 0.05). Compared with P + E group, the percentage of apoptotic cells in CA1 area of the P + E+L group was significantly increased and the percentage of positive cells was remarkably reduced(p < 0.05), the levels of interleukin-1β(IL-1β), interleukin-6(IL-6), interleukin-8(IL-8) and tumor necrosis factor-α(TNF-α) were significantly increased and interleukin-4(IL-4) and interleukin-10(IL-10) was notably reduced(p < 0.05). The protein expression of TLR4 and p-P65 was significantly increased, while the protein expression of p-IκBαwas significantly decreased (p < 0.05). CONCLUSION:Erythropoietin has a protective effect on propofol induced neuropathic injurypropofol in rats, and its mechanism is relevant to the regulation of TLR4/NF-κB signaling pathway.