地黄饮子改善阿尔茨海默病肾虚精亏证大鼠神经炎症的作用机制OACHSSCD

Objective:To investigate the mechanisms of Dihuang Yinzi Decoction on neuroinflammation in rats with Alzheimer's disease(AD)of kidney deficiency and essence depletion syndrome.Methods:Thirty-six rats were randomly divided into a control group,an AD of kidney deficiency and essence depletion syndrome model group,a low-dose Dihuang Yinzi Decoction group,a me-dium-dose Dihuang Yinzi Decoction group,a high-dose Dihuang Yinzi Decoction group,and a donepezil group using a random num-ber table.A combined disease-syndrome model was established by intraperitoneal injection of D-galactose to induce subacute aging in rats,together with bilateral hippocampal CA1 injection of β-amyloid fragment 25-35(Aβ25-3s)to establish an AD model with kid-ney deficiency and essence depletion syndrome.The Morris water maze was used to assess spatial learning and memory ability.Mi-croglial activation was detected by immunofluorescence.The expression levels of β-amyloid 1-42(Aβ1-42)and phosphorylated tau protein 404(pTau404)in the hippocampus were measured by immunohistochemistry.The levels of interleukin-1 β(IL-1 β)and tumor necrosis factor-α(TNF-α)in brain tissue were detected by enzyme-linked immunosorbent assay(ELISA).The protein ex-pression levels of AMP-activated protein kinase(AMPK),phosphorylated AMPK(p-AMPK),nuclear factor-κB p65(NF-κB p65),and phosphorylated NF-κB p65(p-p65)in the hippocampus were detected by Western blot.Results:Dihuang Yinzi Decoction sig-nificantly improved spatial learning and memory ability in AD rats with kidney deficiency and essence depletion syndrome.It im-proved hippocampal neuronal morphology and reduced mitochondrial swelling.The expression of ionized calcium-binding adaptor molecule l(Ibal)was decreased,indicating inhibition of microglial activation.The expression levels of Aβ1-42 and pTau404 were reduced.In addition,p-AMPK protein expression was increased,while p-p65 protein expression was decreased.Conclusion:Di-huang Yinzi Decoction may alleviate neuroinflammation in AD rats with kidney deficiency and essence depletion syndrome by acti-vating the AMPK/NF-κB signaling pathway,thereby exerting anti-AD effects.