The Anti-Inflammatory Of Salidroside In The Inhibition Of Microglia Of DR Through PI3K/AKT Pathway

ObjectiveTo investigate the anti-inflammatory effect of salidroside on microglia of diabetic retinopathy and its mechanism.MethodsAfter one week of accommodation,Forty male SD rats of clean grade were randomly divided into four groups:control group,diabetes group,negative treatment group and SAL group,with 10 rats in each group.Except for the control group,the diabetes models in other groups were established by intraperitoneal injection of 1%STZ-citric acid buffer solution(60mg/kg)at the head,low tail and high position.The control group was treated with intraperitoneal injection of equal volume citric acid buffer.SAL group:salidroside(200mg/kg)was given by gavage every day.Patients in the negative treatment group were given the same volume of normal saline as salidroside by gavage every day.All the rats were given clean with water and feed.After 11 weeks,the samplles were taken for standby.The expressions of IL-6,NF-Bp65 and microglia activity marker IBA-1 in the retina were detected by immunofluorescence assay.The expressions of AKT,p-AKT,and NF-Bp65 in the retina were detected by Western blot.Cell experiment:Immunofluorescence results showed that high glucose promoted the activation of microglia compared with the control group(P<0.01);Compared with the high glucose group,SAL group inhibited the activation of microglia(P<0.01).q PCR results showed that compared with the control group,TNF-α m RNA expression levels of IL-6,IL-1β and TNF-α in the high glucose group were significantly increased(P<0.01).Compared with the high glucose group,the expression levels of IL-6,IL-1β and TNF-α m RNA in the SAL group were decreased(P<0.01).Compared with the SAL group,the expression levels of IL-6,IL-1β and TNF-α m RNA in the inhibitor group were significantly increased(P<0.01),suggesting that SAL could inhibit the inflammatory response of microglia cultured in high glucose medium in vitro and one of the mechanisms might be through PI3K/AKT pathway.ResultsAnimal experiments:Immunofluorescence showed that the expression of IBA-1 was significantly increased in the diabetes group and the negative treatment group compared with the control group(P<0.01).Compared with the diabetic group,the expression of IBA-1 in the SAL group was significantly decreased(P<0.01),indicating that SAL effectively inhibited the activation of DR microglia.Compared with the control group,Western blot results showed that the expression of p-AKT was decreased in the retina of patients in the diabetes group and the negative treatment group(P<0.01),and the expression of NF-Bp65 was increased(P<0.01).Compared with the diabetic group,the expression of p-AKT was increased(P<0.05)and the expression of NF-Bp65 was decreased in the SAL group(P<0.05).Cellular experiment:Immunofluorescence results showed that high glucose promoted the activation of microglia compared with the control group(P<0.01);Compared with the high glucose group,SAL group inhibited the activation of microglia(P<0.01).q PCR results showed that compared with the control group,TNF-α m RNA expression levels of IL-6,IL-1β and TNF-α in the high glucose group were significantly increased(P<0.01).Compared with the high glucose group,the expression levels of IL-6,IL-1β and TNF-α m RNA in the SAL group were decreased(P<0.01).Compared with the SAL group,the expression levels of IL-6,IL-1β and TNF-α m RNA in the inhibitor group were significantly increased(P<0.01),suggesting that SAL could inhibit the inflammatory response of microglia cultured in high glucose medium in vitro and one of the mechanisms might be through PI3K/AKT pathway.ConclusionsSalidroside inhibits the inflammatory response of diabetic retinal microglia,one of the mechanisms may be the anti-inflammatory effect by regulating PI3K/AKT pathway.