Objective:To evaluate the effects of high glucose on hypoxia/reoxygenation-induced injury to the HK-2 cells and the TLR7-MyD88-NF-κB signaling pathway. Methods:The HK-2 cell were randomly divided into 4 groups (n=6):low glucose group (group LG), low glucose and hypoxia/reoxygenation group (group LH/R), high glucose group (group HG), high glucose and hypoxia/reoxygenation group (group HH/R). High glucose and hypoxia/reoxygenation model were established by high glucose stimulation of 72 h, and hypoxia 4 h,reoxygenation 2 h. Cell viability was detected by CCK-8 and LDH release assay. The levels of IL-6 and TNF-α were detected by ELISA, and the expression of TLR7, MyD88 and NF-κB protein in renal cells were detected by immunofluorescence. Results:Compared with the group LG, the activity of CCK-8 was decreased, the expression of LDH, IL-6, TNF-α, TLR7, MyD88 and NF-κB protein were increased in the group NH/R, the group HG and the group HH/R (all P<0.05). Compared with the group LH/R, the expression LDH, IL-6, TLR7, MyD88 and NF-κB protein were increased in the group HG and group HH/R(all P<0.05), the activity of CCK-8 was decreased, the expression of LDH, IL-6, TNF-α, TLR7, MyD88 and NF-κB protein were increased in the group HH/R (all P<0.05). Compared with the group HG, the activity of CCK-8 was decreased in group HG and group HH/R, the expression of LDH, IL-6, TNF-α, TLR7, MyD88 and NF-κB were increased in the group HH/R (all P<0.05). Compared with the HG group, the expression of MyD88 and NF-κB protein were increased in group HH/R (all P<0.05). Conclusion:High glucose is involved in the hypoxia/reoxygenation-induced injury of HK-2 cells through the TLR7/MyD88/NF-κB signaling pathway.
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