Abelmoschus esculentus subfractions attenuate A beta and tau by regulating DPP-4 and insulin resistance signals

doi:10.1186/s12906-020-03163-4

中山醫學大學機構典藏 CSMUIR > 中山醫學大學研究成果 > 期刊論文 > Item 310902500/24367

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/24367

Title:	Abelmoschus esculentus subfractions attenuate A beta and tau by regulating DPP-4 and insulin resistance signals
Authors:	Huang, CN;Wang, CJ;Lin, CL;Li, HH;Yen, AT;Peng, CH
Keywords:	Abelmoschus esculentus;Beta amyloid;Insulin resistance;Dipeptidyl peptidase-4
Date:	2020
Issue Date:	2022-08-09T08:01:08Z (UTC)
Publisher:	BMC
Abstract:	Background Insulin resistance could be associated with the development of Alzheimer disease (AD). The neuropathological hallmarks of AD are beta amyloid (A beta) produced from sequential cleavage initiated by beta-secretase and degraded by insulin degradation enzyme (IDE), as well as hyperphosphorylation of tau (p-tau). Insulin action involves the cascades of insulin receptor substrates (IRS) and phosphatidylinositol 3-kinase (PI3K), while phosphorylation of IRS-1 at ser307 (p-(IRS)-I-ser307-1) hinders the response. Our previous report suggested dipeptidyl peptidase-4 (DPP-4) is crucial to insulin resistance, and the subfractions of Abelmoschus esculentus (AE), F1 and F2, attenuate the signaling. Here we aim to investigate whether AE works to reduce A beta generation via regulating DPP4 and insulin resistance. Methods The subfractions F1 and F2 were prepared according to a succession of procedures. F1 was composed by quercetin glycosides and triterpene ester, and F2 contained a large amount of polysaccharides. The in vitro insulin resistance model was established by SK-N-MC cell line treated with palmitate. MTT was used to define the dose range, and thereby Western blot, ELISA, and the activity assay were used to detect the putative markers. One-way ANOVA was performed for the statistical analysis. Results Treatment of palmitate induced the level of p-(IRS)-I-ser307-1. Both F1 and F2 effectively decrease p-(IRS)-I-ser307-1, and recover the expression of p-PI3K. However, the expression of total IRS plunged with 25 mu g/mL of F1, while descended steadily with 5 mu g/mL of F2. As palmitate increased the levels of A beta 40 and A beta 42, both AE subfractions were effective to reduce A beta generation of and beta-secretase activity, but IDE was not altered in any treatment conditions. The expression of DPP4 was also accompanied with insulin resistance signals. Inhibition of DPP4 attenuated the activity of beta-secretase and production of A beta. Moreover, the present data revealed that both AE subfractions significantly decrease the level of p-Tau. Conclusions In conclusion, we demonstrated that AE would be a potential adjuvant to prevent insulin resistance and the associated pathogenesis of AD, and F2 seems more feasible to be developed.
URI:	http://dx.doi.org/10.1186/s12906-020-03163-4 https://www.webofscience.com/wos/woscc/full-record/WOS:000595395900001 https://ir.csmu.edu.tw:8080/handle/310902500/24367
Relation:	BMC COMPLEMENTARY MEDICINE AND THERAPIES ,2020 ,v20 ,issue 1
Appears in Collections:	[中山醫學大學研究成果] 期刊論文

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