Experimental Study On The Regulation Of TLR4-MyD88-NF-kB Signaling Pathway In Ischemia-reperfusion Of Abdominal Wall Perforator Flap In Rats By Panax Notoginsen

Objective: In clinic,flap transplantation is used to solve soft tissue and skin defects,but poor postoperative flap healing has always been an urgent problem to be solved.In this study,the mechanism of TLR4,My D88 and NF-κB signaling pathway in the rat model of ischemia-reperfusion injury of the abdominal wall flap was observed and studied by modern biotechnology with the help of panax notoginseng.Methods: Sixty SPF SD rats were randomly divided into 4 groups with15 rats in each group,which were group A(sham operation group),group B(model control group),group C(low dose panax notoginseng group)and group D(high dose panax notoginseng group).Sham operation was performed in group A and flap operation was performed in the other three groups.Group A and B were given 0.9% sodium chloride injection intragastric administration,group C and D were given low dose and high dose panax notoginseng intragastric administration,respectively.The survival rate of abdominal flap of rats in each group was observed on the 7th day after operation,and the abdominal wall flap tissue of rats was cut.HE staining and QRTPCR were used to observe the infiltration degree of inflammatory factors and the m RNA expression levels of TLR4,Myd88 and NF-κB.Results:(1)Skin flap survival rate: compared with group A,the wound healing area in group B was significantly decreased(P<0.05),and the skin flap survival rate in groups C and D was improved(P<0.05).(2)HE staining results: Group A: The tissue structure was normal,no inflammatory cell infiltration was observed,and the structural boundaries of each layer were clear.Group B rat skin flap tissue model group: the tissue structure was severely abnormal,collagen fibers were disordered,and many inflammatory cells were visible.Group C: mildly abnormal tissue structure,no obvious collagen fiber and fat cells,disordered connective tissue arrangement,and less of inflammatory cell infiltration.Group D: the tissue structure was abnormal,with many collagen fibers,and the arrangement was relatively orderly.(3)QRT-PCR results: Compared with group A,the m RNA levels of TLR4,My D88 and NF-κB in group B were significantly increased(P<0.05).Compared with group B,the m RNA levels of TLR4,My D88 and NF-κB in group C and D were decreased(P<0.05).Compared with group C,the m RNA levels of TLR4,My D88 and NF-κB in group D of Panax notoginseng were decreased(P<0.05),in a dose-dependent manner.Conclusion: Panax notoginseng can reduce the infiltration of inflammatory cells in the rat model of is CHEMIa-reperfusion injury,reduce the inflammatory response,and improve the survival rate of the rat flap,the mechanism may be related to TLR4,My D88,NF-κB signaling pathway.