File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: 2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside induces autophagy of liver by activating PI3K/Akt and Erk pathway in prediabetic rats

Title2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside induces autophagy of liver by activating PI3K/Akt and Erk pathway in prediabetic rats
Authors
Keywords2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside
Liver injury
Prediabetes
Autophagy
Issue Date2020
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccomplementalternmed/
Citation
BMC Complementary Medicine and Therapies, 2020, v. 20, p. article no. 177 How to Cite?
AbstractBackground: 2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside (TSG) is an active compound derived from Polygonum multiflorum Thunb., a Chinese Taoist herbal medicine, which exerts lipid lowering, anti-cancer, anti-aging, anti-inflammatory and hepatoprotective effects. However, its role in protecting hepatocytes under pre-diabetic condition remains unclear. Methods: In this study, we developed prediabetic SD rats by feeding high-fat and high-sugar diet. The body weight, blood lipid, blood glucose, and fasting insulin (FINS) and insulin resistance index (HOMA-IR) were detected and calculated to assess the potential risk of prediabetes. HE and Oil Red O staining was used, and blood level of biochemical index was detected to observe the liver injury. The autophagic cell death-associated signaling proteins, and the potential signaling factors p-Akt/Akt and p-Erk/Erk were detected using western blot to explore the potential effects of TSG on pre-diabetic liver and the underlying mechanisms. Results: The results showed that the body weight in TSG-treated group was significantly decreased vs. the model group. The blood glucose, the level of FINS and HOMA-IR, TC and TG were decreased in TSG-treated group as well. Furthermore, TSG treatment significantly ameliorated lipid droplet accumulation, enhanced liver anti-oxidative response which may be associated with an increased activity of SOD and GSH-Px, and a decrease of LDLC and MDA. The autophagic cell death-associated proteins, p-AMPK, ATG12, LC3 II, and Beclin 1 were up-regulated in the TSG-treated group, while the upstream signaling pathway, PI3K/Akt and Erk, were activated. Conclusions: TSG induced liver autophagic cell death to protect liver from prediabetic injury by activating PI3K/Akt and Erk.
Persistent Identifierhttp://hdl.handle.net/10722/284277
ISSN
2023 Impact Factor: 3.3
2023 SCImago Journal Rankings: 0.673
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWANG, X-
dc.contributor.authorZENG, J-
dc.contributor.authorWANG, X-
dc.contributor.authorLI, J-
dc.contributor.authorCHEN, J-
dc.contributor.authorWang, N-
dc.contributor.authorZHANG, M-
dc.contributor.authorFeng, Y-
dc.contributor.authorGUO, H-
dc.date.accessioned2020-07-20T05:57:27Z-
dc.date.available2020-07-20T05:57:27Z-
dc.date.issued2020-
dc.identifier.citationBMC Complementary Medicine and Therapies, 2020, v. 20, p. article no. 177-
dc.identifier.issn2662-7671-
dc.identifier.urihttp://hdl.handle.net/10722/284277-
dc.description.abstractBackground: 2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside (TSG) is an active compound derived from Polygonum multiflorum Thunb., a Chinese Taoist herbal medicine, which exerts lipid lowering, anti-cancer, anti-aging, anti-inflammatory and hepatoprotective effects. However, its role in protecting hepatocytes under pre-diabetic condition remains unclear. Methods: In this study, we developed prediabetic SD rats by feeding high-fat and high-sugar diet. The body weight, blood lipid, blood glucose, and fasting insulin (FINS) and insulin resistance index (HOMA-IR) were detected and calculated to assess the potential risk of prediabetes. HE and Oil Red O staining was used, and blood level of biochemical index was detected to observe the liver injury. The autophagic cell death-associated signaling proteins, and the potential signaling factors p-Akt/Akt and p-Erk/Erk were detected using western blot to explore the potential effects of TSG on pre-diabetic liver and the underlying mechanisms. Results: The results showed that the body weight in TSG-treated group was significantly decreased vs. the model group. The blood glucose, the level of FINS and HOMA-IR, TC and TG were decreased in TSG-treated group as well. Furthermore, TSG treatment significantly ameliorated lipid droplet accumulation, enhanced liver anti-oxidative response which may be associated with an increased activity of SOD and GSH-Px, and a decrease of LDLC and MDA. The autophagic cell death-associated proteins, p-AMPK, ATG12, LC3 II, and Beclin 1 were up-regulated in the TSG-treated group, while the upstream signaling pathway, PI3K/Akt and Erk, were activated. Conclusions: TSG induced liver autophagic cell death to protect liver from prediabetic injury by activating PI3K/Akt and Erk.-
dc.languageeng-
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccomplementalternmed/-
dc.relation.ispartofBMC Complementary Medicine and Therapies-
dc.rightsBMC Complementary Medicine and Therapies. Copyright © BioMed Central Ltd.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subject2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside-
dc.subjectLiver injury-
dc.subjectPrediabetes-
dc.subjectAutophagy-
dc.title2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside induces autophagy of liver by activating PI3K/Akt and Erk pathway in prediabetic rats-
dc.typeArticle-
dc.identifier.emailWang, N: ckwang@hku.hk-
dc.identifier.emailFeng, Y: yfeng@hku.hk-
dc.identifier.authorityWang, N=rp02075-
dc.identifier.authorityFeng, Y=rp00466-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/s12906-020-02949-w-
dc.identifier.pmid32513151-
dc.identifier.pmcidPMC7278085-
dc.identifier.scopuseid_2-s2.0-85097037466-
dc.identifier.hkuros311480-
dc.identifier.volume20-
dc.identifier.spagearticle no. 177-
dc.identifier.epagearticle no. 177-
dc.identifier.isiWOS:000550369900001-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl2662-7671-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats