Neuroprotective Effects of Ginsenoside Rg1 against Hyperphosphorylated Tau-Induced Diabetic Retinal Neurodegeneration via Activation of IRS-1/Akt/GSK3β Signaling

• DOI: 10.1021/acs.jafc.9b02954
• Publication Date: 2019-07-14T14:04:04Z
• Authors: Ying Ying; Yi-lin Zhang; Can-jie Ma; Mei-qi Li; Chao-yue Tang; Yang-fan Yang; Jun-hui Zeng; Xiao-yan Huang; Junbo Yi; Xiao-mei Wang; Zhen-dan He; Xing-sheng Shu
• Keywords: Hyperphosphorylation; Panax notoginseng

We have recently demonstrated that tau hyperphosphorylation causes diabetic synaptic neurodegeneration of retinal ganglion cells (RGCs), which might be the earliest affair during pathogenesis retinopathy (DR). Thus, there is a pressing need to seek therapeutic agents possessing neuroprotective effects against in RGCs for arresting progression DR. Here, using well-characterized diabetes model db/db mouse, we discovered topical ocular application 10 mg/kg/day ginsenoside Rg1 (GRg1), one major active ingredients extracted from Panax ginseng and notoginseng, ameliorated hyperphosphorylated tau-triggered mice. The GRg1 on retinae were abrogated when IRS-1 or Akt was suppressed by intravitreal injection with si-IRS-1 topically coadministered specific inhibitor Akt, respectively. However, selective repression GSK3β administration si-GSK3β rescued properties inactivated. Therefore, present study showed first time can prevent tau-induced via activation IRS-1/Akt/GSK3β signaling early phase Moreover, our data clarify potential significance intervention strategies