Lycium barbarum glycopeptide ameliorates aging phenotypes and enhances cardiac metabolism by activating the PINK1/Parkin-mediated mitophagy pathway in D-galactose-induced mice

Background: Aging is a complex biological process that disrupts tissue structure and impairs physiological function, which contributes to the development of age-related diseases such as cardiovascular disorders. However, effective treatment strategies are lacking. Objective: To investigate the gerop...

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Main Authors: Tianchan Peng, Jian Xiang, Yun Tian, Xiaogen Tang, Lina Wang, Lijuan Gao, Oscar Junhong Luo, Li’an Huang, Guobing Chen
Format: Article
Language:English
Published: Elsevier 2025-02-01
Series:Experimental Gerontology
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Online Access:http://www.sciencedirect.com/science/article/pii/S0531556525000142
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author Tianchan Peng
Jian Xiang
Yun Tian
Xiaogen Tang
Lina Wang
Lijuan Gao
Oscar Junhong Luo
Li’an Huang
Guobing Chen
author_facet Tianchan Peng
Jian Xiang
Yun Tian
Xiaogen Tang
Lina Wang
Lijuan Gao
Oscar Junhong Luo
Li’an Huang
Guobing Chen
author_sort Tianchan Peng
collection DOAJ
description Background: Aging is a complex biological process that disrupts tissue structure and impairs physiological function, which contributes to the development of age-related diseases such as cardiovascular disorders. However, effective treatment strategies are lacking. Objective: To investigate the geroprotective effects of Lycium barbarum glycopeptide (LbGp) and its potential mechanisms in a D-galactose-induced accelerated aging mouse model. Methods: Mice were subcutaneously injected with D-galactose (500 mg/kg/day) for 12 weeks to induce aging, while LbGp was orally administered (100 mg/kg/day) throughout the study. The geroprotective effects of LbGp were assessed by behavioral tests, cardiac echocardiography, pathohistological and transcriptomic analyses. Transmission electron microscopy was used to observe the ultrastructure of mitochondria. Mitochondrial stress assays and JC-1 fluorescent probe were conducted to evaluate mitochondrial function. Flow cytometer and western blot were performed to assess mitophagy flux. Results: LbGp treatment improved the aging phenotypes of D-galactose-induced mice, with a pronounced enhancement in cardiac function compared to neurocognitive and skeletal muscle functions. Transcriptome analysis indicated that LbGp ameliorated energy metabolism in the heart. Mitochondrial assays revealed LbGp improved mitochondrial function and preserved structural integrity of the mitochondrial inner membrane. LbGp attenuated mitochondrial fission and restored impaired PINK1/Parkin-mediated mitophagy pathway caused by D-galactose in cardiomyocytes. Conclusion: LbGp can ameliorate aging phenotypes and enhance cardiac metabolism by activating the PINK1/Parkin-mediated mitophagy pathway in D-galactose-induced mice. These findings underscore its potential as a therapeutic agent for aging and aging-related cardiovascular diseases.
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spelling doaj-art-732b0fc8ed8343c48dba04088e4e45152025-01-31T05:10:09ZengElsevierExperimental Gerontology1873-68152025-02-01200112686Lycium barbarum glycopeptide ameliorates aging phenotypes and enhances cardiac metabolism by activating the PINK1/Parkin-mediated mitophagy pathway in D-galactose-induced miceTianchan Peng0Jian Xiang1Yun Tian2Xiaogen Tang3Lina Wang4Lijuan Gao5Oscar Junhong Luo6Li’an Huang7Guobing Chen8Department of Neurology, Affiliated Hospital of Jinan University, Guangzhou 510632, China; Department of Microbiology and Immunology, School of Medicine; Institute of Geriatric Immunology, School of Medicine, Jinan University, Guangzhou 510632, ChinaDepartment of Microbiology and Immunology, School of Medicine; Institute of Geriatric Immunology, School of Medicine, Jinan University, Guangzhou 510632, China; Key Laboratory of Viral Pathogenesis & Infection Prevention and Control (Jinan University), Ministry of Education, Guangzhou 510632, China; Guangdong-Hong Kong-Macau Great Bay Area Geroscience Joint Laboratory, School of Medicine, Jinan University, Guangzhou 510632, ChinaDepartment of Microbiology and Immunology, School of Medicine; Institute of Geriatric Immunology, School of Medicine, Jinan University, Guangzhou 510632, China; Key Laboratory of Viral Pathogenesis & Infection Prevention and Control (Jinan University), Ministry of Education, Guangzhou 510632, China; Guangdong-Hong Kong-Macau Great Bay Area Geroscience Joint Laboratory, School of Medicine, Jinan University, Guangzhou 510632, ChinaDepartment of Microbiology and Immunology, School of Medicine; Institute of Geriatric Immunology, School of Medicine, Jinan University, Guangzhou 510632, China; Key Laboratory of Viral Pathogenesis & Infection Prevention and Control (Jinan University), Ministry of Education, Guangzhou 510632, China; Guangdong-Hong Kong-Macau Great Bay Area Geroscience Joint Laboratory, School of Medicine, Jinan University, Guangzhou 510632, ChinaDepartment of Neurology, Affiliated Hospital of Jinan University, Guangzhou 510632, China; Department of Microbiology and Immunology, School of Medicine; Institute of Geriatric Immunology, School of Medicine, Jinan University, Guangzhou 510632, ChinaDepartment of Microbiology and Immunology, School of Medicine; Institute of Geriatric Immunology, School of Medicine, Jinan University, Guangzhou 510632, China; Key Laboratory of Viral Pathogenesis & Infection Prevention and Control (Jinan University), Ministry of Education, Guangzhou 510632, China; Guangdong-Hong Kong-Macau Great Bay Area Geroscience Joint Laboratory, School of Medicine, Jinan University, Guangzhou 510632, China; Zhuhai Institute of Jinan University, Zhuhai 519070, ChinaDepartment of Microbiology and Immunology, School of Medicine; Institute of Geriatric Immunology, School of Medicine, Jinan University, Guangzhou 510632, China; Key Laboratory of Viral Pathogenesis & Infection Prevention and Control (Jinan University), Ministry of Education, Guangzhou 510632, China; Guangdong-Hong Kong-Macau Great Bay Area Geroscience Joint Laboratory, School of Medicine, Jinan University, Guangzhou 510632, China; Zhuhai Institute of Jinan University, Zhuhai 519070, ChinaDepartment of Neurology, Affiliated Hospital of Jinan University, Guangzhou 510632, China; Correspondence to: L. Huang, Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.Department of Microbiology and Immunology, School of Medicine; Institute of Geriatric Immunology, School of Medicine, Jinan University, Guangzhou 510632, China; Key Laboratory of Viral Pathogenesis & Infection Prevention and Control (Jinan University), Ministry of Education, Guangzhou 510632, China; Guangdong-Hong Kong-Macau Great Bay Area Geroscience Joint Laboratory, School of Medicine, Jinan University, Guangzhou 510632, China; Zhuhai Institute of Jinan University, Zhuhai 519070, China; Correspondence to: G. Chen, Jinan University, Guangzhou, Guangdong, China.Background: Aging is a complex biological process that disrupts tissue structure and impairs physiological function, which contributes to the development of age-related diseases such as cardiovascular disorders. However, effective treatment strategies are lacking. Objective: To investigate the geroprotective effects of Lycium barbarum glycopeptide (LbGp) and its potential mechanisms in a D-galactose-induced accelerated aging mouse model. Methods: Mice were subcutaneously injected with D-galactose (500 mg/kg/day) for 12 weeks to induce aging, while LbGp was orally administered (100 mg/kg/day) throughout the study. The geroprotective effects of LbGp were assessed by behavioral tests, cardiac echocardiography, pathohistological and transcriptomic analyses. Transmission electron microscopy was used to observe the ultrastructure of mitochondria. Mitochondrial stress assays and JC-1 fluorescent probe were conducted to evaluate mitochondrial function. Flow cytometer and western blot were performed to assess mitophagy flux. Results: LbGp treatment improved the aging phenotypes of D-galactose-induced mice, with a pronounced enhancement in cardiac function compared to neurocognitive and skeletal muscle functions. Transcriptome analysis indicated that LbGp ameliorated energy metabolism in the heart. Mitochondrial assays revealed LbGp improved mitochondrial function and preserved structural integrity of the mitochondrial inner membrane. LbGp attenuated mitochondrial fission and restored impaired PINK1/Parkin-mediated mitophagy pathway caused by D-galactose in cardiomyocytes. Conclusion: LbGp can ameliorate aging phenotypes and enhance cardiac metabolism by activating the PINK1/Parkin-mediated mitophagy pathway in D-galactose-induced mice. These findings underscore its potential as a therapeutic agent for aging and aging-related cardiovascular diseases.http://www.sciencedirect.com/science/article/pii/S0531556525000142AgingLycium barbarum glycopeptideD-galactoseCardiac metabolismMitophagy
spellingShingle Tianchan Peng
Jian Xiang
Yun Tian
Xiaogen Tang
Lina Wang
Lijuan Gao
Oscar Junhong Luo
Li’an Huang
Guobing Chen
Lycium barbarum glycopeptide ameliorates aging phenotypes and enhances cardiac metabolism by activating the PINK1/Parkin-mediated mitophagy pathway in D-galactose-induced mice
Experimental Gerontology
Aging
Lycium barbarum glycopeptide
D-galactose
Cardiac metabolism
Mitophagy
title Lycium barbarum glycopeptide ameliorates aging phenotypes and enhances cardiac metabolism by activating the PINK1/Parkin-mediated mitophagy pathway in D-galactose-induced mice
title_full Lycium barbarum glycopeptide ameliorates aging phenotypes and enhances cardiac metabolism by activating the PINK1/Parkin-mediated mitophagy pathway in D-galactose-induced mice
title_fullStr Lycium barbarum glycopeptide ameliorates aging phenotypes and enhances cardiac metabolism by activating the PINK1/Parkin-mediated mitophagy pathway in D-galactose-induced mice
title_full_unstemmed Lycium barbarum glycopeptide ameliorates aging phenotypes and enhances cardiac metabolism by activating the PINK1/Parkin-mediated mitophagy pathway in D-galactose-induced mice
title_short Lycium barbarum glycopeptide ameliorates aging phenotypes and enhances cardiac metabolism by activating the PINK1/Parkin-mediated mitophagy pathway in D-galactose-induced mice
title_sort lycium barbarum glycopeptide ameliorates aging phenotypes and enhances cardiac metabolism by activating the pink1 parkin mediated mitophagy pathway in d galactose induced mice
topic Aging
Lycium barbarum glycopeptide
D-galactose
Cardiac metabolism
Mitophagy
url http://www.sciencedirect.com/science/article/pii/S0531556525000142
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