Expression of TLR2 mRNA and TLR4 mRNA in renal tissues of rats with endotoxin-induced shock / 上海交通大学学报（医学版）

ABSTRACT

Objective To investigate the expression of Toll like receptor 2 (TLR2) mRNA and TLR4 mRNA in renal tissues of rats with endotoxin-induced shock, and explore the possible effects and mechanism of vasoactive intestinal peptide (VIP) and methylprednisolone ( MP) on renal injury. Methods Endotoxin (E coli O55 B5 LPS, 10 mg/kg) was injected intravenously to the rats to establish the endotoxin-induced shock models ( LPS group, n = 16). The rats in LPS + VIP group (n = 16) was injected with VIP (5 nmol/kg) after model establishment, and those in LPS + VIP + MP group (n = 16) was injected with VIP (5 nmol/kg) and MP (3 mg/kg) after model establishment. Besides, normal saline control group (control group) was established( n = 8). Electron microscope was used to observe the histopathological changes in renal tissues 6 h and 24 h after model establishment, and RT-PCR was performed to evaluate the expression of TLR2 mRNA and TLR4 mRNA in renal tissues. Results Six h after model establishment, glomerular endothelial cell swelling and vacuolar degeneration of mitochondria were observed in LPS group under electronic microscope. Twenty-four h after model establishment, mitochondrial swelling, vacuolar degeneration and slight nucleus pyknosis of renal tubular cells were observed in LPS group. The renal pathological changes in LPS + VIP group and LPS + VIP + MP group were much less severe than those in LPS group at the same time. The expression of TLR2 mRNA and TLR4 mRNA in LPS, LPS + VIP and LPS + VIP + MP groups was significantly higher than that in control group 6 h after LPS injection (P <0.01), while the expression of TLR2 mRNA and TLR4 mRNA in LPS group was higher than that in the other groups 24 h after LPS injection (P < 0.01) . Conclusion The expression of TLR2 mRNA and TLR4 mRNA in renal tissues of rats with endotoxin-induced shock is markedly up-regulated. VIP and MP can obviously alleviate renal pathological changes, and the mechanism may contribute to impacting on the expression of TLR2 mRNA and TLR4 mRNA.