1.Urolithin A improves motor function and attenuates muscle fibrosis in a mouse model of Duchenne muscular dystrophy
Hongyi JIA ; Chaoming QIU ; Dan LIU ; Luchen SHAN ; Pei YU ; Xifei YANG
Chinese Journal of Pathophysiology 2025;41(11):2184-2190
AIM:To investigate the effects of urolithin A on motor function and muscle fibrosis in dystrophin-deficient mdx mice,a model of Duchenne muscular dystrophy.METHODS:Twelve 26-week-old SPF male dystrophin gene deficient C57BL/10ScSnJNju-Dmdem3Cd4/Gpt(mdx)mice were randomly divided into model group and urolithin A treatment group,with 6 mice in each group.Additionally,six wild-type SPF male mice were selected as the normal con-trol.The motor ability of the mice was evaluated by pole climbing test,inverted suspension test,grip strength test and en-durance test.The body mass,mitochondrial relative copy number,ATP level and malondialdehyde(MDA)level were compared among the mice in different groups.Hematoxylin-eosin staining,Masson staining and immunohistochemistry were performed to analyze the atrophy and pathological changes of the gastrocnemius muscle.RESULTS:Compared with normal control group,the mdx mice in model group exhibited significantly impaired motor function,as evidenced by pro-longed pole-climbing time(P<0.01),reduced suspension time and forelimb/hindlimb grip strength(P<0.01),and in-creased number of electrical stimuli required to induce movement(P<0.01).Additionally,mitochondrial relative copy number and ATP level were significantly decreased(P<0.01),while MDA level was significantly elevated(P<0.01).Histological analysis revealed marked inflammatory cell infiltration and extensive tissue fibrosis in the gastrocnemius mus-cle.In contrast,urolithin A treatment significantly improved motor performance(P<0.01),attenuated inflammatory cell infiltration and muscle fibrosis,increased mitochondrial copy number,restored ATP level(P<0.05),and reduced MDA level(P<0.01).CONCLUSION:Urolithin A ameliorates motor dysfunction and alleviates muscle fibrosis in mdx mice,suggesting its potential therapeutic benefits for Duchenne muscular dystrophy.
2.Urolithin A improves motor function and attenuates muscle fibrosis in a mouse model of Duchenne muscular dystrophy
Hongyi JIA ; Chaoming QIU ; Dan LIU ; Luchen SHAN ; Pei YU ; Xifei YANG
Chinese Journal of Pathophysiology 2025;41(11):2184-2190
AIM:To investigate the effects of urolithin A on motor function and muscle fibrosis in dystrophin-deficient mdx mice,a model of Duchenne muscular dystrophy.METHODS:Twelve 26-week-old SPF male dystrophin gene deficient C57BL/10ScSnJNju-Dmdem3Cd4/Gpt(mdx)mice were randomly divided into model group and urolithin A treatment group,with 6 mice in each group.Additionally,six wild-type SPF male mice were selected as the normal con-trol.The motor ability of the mice was evaluated by pole climbing test,inverted suspension test,grip strength test and en-durance test.The body mass,mitochondrial relative copy number,ATP level and malondialdehyde(MDA)level were compared among the mice in different groups.Hematoxylin-eosin staining,Masson staining and immunohistochemistry were performed to analyze the atrophy and pathological changes of the gastrocnemius muscle.RESULTS:Compared with normal control group,the mdx mice in model group exhibited significantly impaired motor function,as evidenced by pro-longed pole-climbing time(P<0.01),reduced suspension time and forelimb/hindlimb grip strength(P<0.01),and in-creased number of electrical stimuli required to induce movement(P<0.01).Additionally,mitochondrial relative copy number and ATP level were significantly decreased(P<0.01),while MDA level was significantly elevated(P<0.01).Histological analysis revealed marked inflammatory cell infiltration and extensive tissue fibrosis in the gastrocnemius mus-cle.In contrast,urolithin A treatment significantly improved motor performance(P<0.01),attenuated inflammatory cell infiltration and muscle fibrosis,increased mitochondrial copy number,restored ATP level(P<0.05),and reduced MDA level(P<0.01).CONCLUSION:Urolithin A ameliorates motor dysfunction and alleviates muscle fibrosis in mdx mice,suggesting its potential therapeutic benefits for Duchenne muscular dystrophy.
3.The research progress of traditional Chinese medicine nursing intervention on the rehabilitation of patients with cervical spondylosis
Jinwei BIAN ; Xulin LI ; Longhai QIU ; Shanji WU ; Chaoming YANG ; Pengfei DONG ; Naping LUO ; Qu SHEN
Chinese Journal of Practical Nursing 2018;34(30):2394-2397
Cervical spondylosis belongs to the category of "arthralgia syndrome" in traditional Chinese medicine.From the number and distribution range of disease,the incidence of cervical spondylosis is yearly increasing and shows a trend of younger age.Cervical spondylosis has become one of the common diseases that seriously affect people's health.This article reviews the relevant literature of TCM nursing interventions in the rehabilitation of cervical spondylosis and explores the influence of TCM nursing interventions on patients with cervical spondylosis including tuina,cupping,moxibustion,scrapping,TCM fumigation,auricular therapy and so on,in order to provide a reference for the future practice and research of TCM nursing interventions for patients with cervical spondylosis.
4.Adeno-associated virus mediated T-bet gene transfer into SGC-7901 cell to regulate IFN-gamma production.
Gufeng QIU ; Suoying WANG ; Shengjun WANG ; Qixiang SHAO ; Jie MA ; Ming YANG ; Xiaopeng XU ; Chaoming MAO ; Zhaoliang SU ; Xinxiang HUANG ; Huaxi XU
Journal of Biomedical Engineering 2009;26(3):606-619
In order to investigate the effect of T-bet on malignant cells, we selected SGC-7901, a kind of human gastric carcinoma cell line, and used gene clone technique and adeno-associated virus (AAV) packing technology, thus obtaining a recombinant rAAV-eGFP-T-bet and T-bet gene-transfected SGC-7901 cells. Then the function of T-bet gene-infected SGC-7901 cells was researched by detecting the levels of IFN-gamma and T-bet production. The results showed: (1) It was verified that rAAV-T-bet's packing was completed; (2) After SGC-7901 cells was transfected by rAAV-eGFP-T-bet, a green fluorescence was found in about 30%-40% SGC-7901s, and the gene of 1670 bp (T-bet) and 388 bp (IFN-gamma) were generated from SGC-7901s cells; (3) The proteins of IFN-gamma and T-bet secreted by SGC-7901 cells were also detected. These reveal that SGC-7901 cell is efficiently infected by rAAV encoding T-bet, which can induce transfected cells to secret IFN-gamma. It may be useful in the researches on cancer immune therapy of transfecting T-bet gene.
Cell Line, Tumor
;
Dependovirus
;
genetics
;
metabolism
;
Green Fluorescent Proteins
;
biosynthesis
;
Humans
;
Interferon-gamma
;
biosynthesis
;
Recombinant Proteins
;
biosynthesis
;
genetics
;
Stomach Neoplasms
;
genetics
;
metabolism
;
T-Box Domain Proteins
;
biosynthesis
;
genetics
;
Transfection

Result Analysis
Print
Save
E-mail