Buyang Huanwu Decoction reduces mitochondrial autophagy in rheumatoid arthritis synovial fibroblasts in hypoxic culture by inhibiting the BNIP3-PI3K/Akt pathway
To investigate the role of the BNIP3-PI3K/Akt signaling pathway in mediating the inhibitory effect of Decoction (BYHWT) on mitochondrial autophagy in human synovial fibroblasts from rheumatoid arthritis patients (FLS-RA) cultured under a hypoxic condition. Forty normal Wistar rats were randomized in...
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| Veröffentlicht in: | Nan fang yi ke da xue xue bao = Journal of Southern Medical University 2025-01, Vol.45 (1), p.35 |
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| container_title | Nan fang yi ke da xue xue bao = Journal of Southern Medical University |
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| creator | Zhan, Junping Huang, Shuo Meng, Qingliang Fan, Wei Gu, Huimin Cui, Jiakang Wang, Huilian |
| description | To investigate the role of the BNIP3-PI3K/Akt signaling pathway in mediating the inhibitory effect of
Decoction (BYHWT) on mitochondrial autophagy in human synovial fibroblasts from rheumatoid arthritis patients (FLS-RA) cultured under a hypoxic condition.
Forty normal Wistar rats were randomized into two groups (
=20) for daily gavage of BYHWT or distilled water for 7 days to prepare BYHWT-medicated or control sera. FLS-RA were cultured in routine condition or exposed to hypoxia (10% O
) for 24 h wigh subsequent treatment with IL-1β, followed by treatment with diluted BYHWT-medicated serum (5%, 10% and 20%) or control serum. AnnexinV-APC/7-AAD double staining and T-AOC kit were used for detecting apoptosis and total antioxidant capacity of the cells, and the changes in ROS, ATP level, mitochondrial membrane potential and Ca
homeostasis were analyzed. The changes in mRNA and protein expressions of BNIP3, PI3K and AKT and mRNA expressions of LC3, Beclin-1 and P62 were detected using RT-qPCR and Western blotting.
Treatment with BYHWT-medicated serum dose-dependently lowered apoptosis rate of IL-1β-induced FLS-RA with hypoxic exposure. The treatment significantly decreased T-AOC concentration, increased ROS production, autophagosome formation and ATPase levels, and lowered mitochondrial membrane potential and Ca
level in the cells. In IL-1β-induced FLS-RA with hypoxic exposure, treatment with BYHWT-medicated serum significantly increased BNIP3 protein expression, decreased the protein expressions of PI3K and AKT, increased the mRNA expressions of BNIP3 and P62, and lowered the mRNA expressions of PI3K, AKT, LC3 and Beclin-1 without significantly affecting Beclin-1 protein expression. The cells treated with 5% and 10% BYHWT-medicated serum showed no significant changes in LC3 expression.
BYHWT inhibits mitochondrial autophagy in IL-1β-induced FLS-RA with hypoxic exposure possibly by inhibiting BNIP3-mediated PI3K/AKT signaling pathway. |
| doi_str_mv | 10.12122/j.issn.1673-4254.2025.01.05 |
| format | Article |
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Decoction (BYHWT) on mitochondrial autophagy in human synovial fibroblasts from rheumatoid arthritis patients (FLS-RA) cultured under a hypoxic condition.
Forty normal Wistar rats were randomized into two groups (
=20) for daily gavage of BYHWT or distilled water for 7 days to prepare BYHWT-medicated or control sera. FLS-RA were cultured in routine condition or exposed to hypoxia (10% O
) for 24 h wigh subsequent treatment with IL-1β, followed by treatment with diluted BYHWT-medicated serum (5%, 10% and 20%) or control serum. AnnexinV-APC/7-AAD double staining and T-AOC kit were used for detecting apoptosis and total antioxidant capacity of the cells, and the changes in ROS, ATP level, mitochondrial membrane potential and Ca
homeostasis were analyzed. The changes in mRNA and protein expressions of BNIP3, PI3K and AKT and mRNA expressions of LC3, Beclin-1 and P62 were detected using RT-qPCR and Western blotting.
Treatment with BYHWT-medicated serum dose-dependently lowered apoptosis rate of IL-1β-induced FLS-RA with hypoxic exposure. The treatment significantly decreased T-AOC concentration, increased ROS production, autophagosome formation and ATPase levels, and lowered mitochondrial membrane potential and Ca
level in the cells. In IL-1β-induced FLS-RA with hypoxic exposure, treatment with BYHWT-medicated serum significantly increased BNIP3 protein expression, decreased the protein expressions of PI3K and AKT, increased the mRNA expressions of BNIP3 and P62, and lowered the mRNA expressions of PI3K, AKT, LC3 and Beclin-1 without significantly affecting Beclin-1 protein expression. The cells treated with 5% and 10% BYHWT-medicated serum showed no significant changes in LC3 expression.
BYHWT inhibits mitochondrial autophagy in IL-1β-induced FLS-RA with hypoxic exposure possibly by inhibiting BNIP3-mediated PI3K/AKT signaling pathway.</description><identifier>ISSN: 1673-4254</identifier><identifier>DOI: 10.12122/j.issn.1673-4254.2025.01.05</identifier><identifier>PMID: 39819710</identifier><language>chi ; eng</language><publisher>China</publisher><subject>Animals ; Apoptosis - drug effects ; Arthritis, Rheumatoid - drug therapy ; Arthritis, Rheumatoid - metabolism ; Autophagy - drug effects ; Cells, Cultured ; Drugs, Chinese Herbal - pharmacology ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Humans ; Interleukin-1beta - metabolism ; Male ; Membrane Proteins - metabolism ; Mitochondria - drug effects ; Mitochondria - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Wistar ; Signal Transduction - drug effects ; Synovial Membrane - cytology ; Synovial Membrane - drug effects ; Synovial Membrane - metabolism</subject><ispartof>Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025-01, Vol.45 (1), p.35</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39819710$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhan, Junping</creatorcontrib><creatorcontrib>Huang, Shuo</creatorcontrib><creatorcontrib>Meng, Qingliang</creatorcontrib><creatorcontrib>Fan, Wei</creatorcontrib><creatorcontrib>Gu, Huimin</creatorcontrib><creatorcontrib>Cui, Jiakang</creatorcontrib><creatorcontrib>Wang, Huilian</creatorcontrib><title>Buyang Huanwu Decoction reduces mitochondrial autophagy in rheumatoid arthritis synovial fibroblasts in hypoxic culture by inhibiting the BNIP3-PI3K/Akt pathway</title><title>Nan fang yi ke da xue xue bao = Journal of Southern Medical University</title><addtitle>Nan Fang Yi Ke Da Xue Xue Bao</addtitle><description>To investigate the role of the BNIP3-PI3K/Akt signaling pathway in mediating the inhibitory effect of
Decoction (BYHWT) on mitochondrial autophagy in human synovial fibroblasts from rheumatoid arthritis patients (FLS-RA) cultured under a hypoxic condition.
Forty normal Wistar rats were randomized into two groups (
=20) for daily gavage of BYHWT or distilled water for 7 days to prepare BYHWT-medicated or control sera. FLS-RA were cultured in routine condition or exposed to hypoxia (10% O
) for 24 h wigh subsequent treatment with IL-1β, followed by treatment with diluted BYHWT-medicated serum (5%, 10% and 20%) or control serum. AnnexinV-APC/7-AAD double staining and T-AOC kit were used for detecting apoptosis and total antioxidant capacity of the cells, and the changes in ROS, ATP level, mitochondrial membrane potential and Ca
homeostasis were analyzed. The changes in mRNA and protein expressions of BNIP3, PI3K and AKT and mRNA expressions of LC3, Beclin-1 and P62 were detected using RT-qPCR and Western blotting.
Treatment with BYHWT-medicated serum dose-dependently lowered apoptosis rate of IL-1β-induced FLS-RA with hypoxic exposure. The treatment significantly decreased T-AOC concentration, increased ROS production, autophagosome formation and ATPase levels, and lowered mitochondrial membrane potential and Ca
level in the cells. In IL-1β-induced FLS-RA with hypoxic exposure, treatment with BYHWT-medicated serum significantly increased BNIP3 protein expression, decreased the protein expressions of PI3K and AKT, increased the mRNA expressions of BNIP3 and P62, and lowered the mRNA expressions of PI3K, AKT, LC3 and Beclin-1 without significantly affecting Beclin-1 protein expression. The cells treated with 5% and 10% BYHWT-medicated serum showed no significant changes in LC3 expression.
BYHWT inhibits mitochondrial autophagy in IL-1β-induced FLS-RA with hypoxic exposure possibly by inhibiting BNIP3-mediated PI3K/AKT signaling pathway.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Arthritis, Rheumatoid - drug therapy</subject><subject>Arthritis, Rheumatoid - metabolism</subject><subject>Autophagy - drug effects</subject><subject>Cells, Cultured</subject><subject>Drugs, Chinese Herbal - pharmacology</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>Humans</subject><subject>Interleukin-1beta - metabolism</subject><subject>Male</subject><subject>Membrane Proteins - metabolism</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Signal Transduction - drug effects</subject><subject>Synovial Membrane - cytology</subject><subject>Synovial Membrane - drug effects</subject><subject>Synovial Membrane - metabolism</subject><issn>1673-4254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo90MtO3DAUBmAvqADBvALyootukvE1iZdAL4yKgAX70bHjTDxN4tQXaN6mj8qMSlkd6ej7_yMdhD5TUlJGGVvvSxfjVNKq5oVgUpSMMFkSWhJ5gs4_1mdoFeOeEMIU41TIU3TGVUNVTck5-nuTF5h2-C7D9JrxV2u8Sc5PONg2Gxvx6JI3vZ_a4GDAkJOfe9gt2B1Ib_MIybsWQ0h9cMlFHJfJvxxp53TweoCY4hH3y-z_OINNHlIOFutjRe_0IXQ4n3qLbx42T7x42vCf6-tfCc-Q-ldYLtGnDoZoV-_zAj1___Z8e1fcP_7Y3F7fF7OsSNHySmpQhtVWc8K1YBpkpaWoOtFUmjTMGAac81arWtRE14YpoUCrTvCmU_wCfflXOwf_O9uYtqOLxg4DTNbnuOVUVrVqeC0P9OqdZj3adjsHN0JYtv-fyt8Aw8R-dg</recordid><startdate>20250120</startdate><enddate>20250120</enddate><creator>Zhan, Junping</creator><creator>Huang, Shuo</creator><creator>Meng, Qingliang</creator><creator>Fan, Wei</creator><creator>Gu, Huimin</creator><creator>Cui, Jiakang</creator><creator>Wang, Huilian</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20250120</creationdate><title>Buyang Huanwu Decoction reduces mitochondrial autophagy in rheumatoid arthritis synovial fibroblasts in hypoxic culture by inhibiting the BNIP3-PI3K/Akt pathway</title><author>Zhan, Junping ; Huang, Shuo ; Meng, Qingliang ; Fan, Wei ; Gu, Huimin ; Cui, Jiakang ; Wang, Huilian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p560-d365ba9c27eb303b42ba56b546f486b082cc2a333db97470b7c2949ab9f438f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>chi ; eng</language><creationdate>2025</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Arthritis, Rheumatoid - drug therapy</topic><topic>Arthritis, Rheumatoid - metabolism</topic><topic>Autophagy - drug effects</topic><topic>Cells, Cultured</topic><topic>Drugs, Chinese Herbal - pharmacology</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>Humans</topic><topic>Interleukin-1beta - metabolism</topic><topic>Male</topic><topic>Membrane Proteins - metabolism</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Signal Transduction - drug effects</topic><topic>Synovial Membrane - cytology</topic><topic>Synovial Membrane - drug effects</topic><topic>Synovial Membrane - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>Zhan, Junping</creatorcontrib><creatorcontrib>Huang, Shuo</creatorcontrib><creatorcontrib>Meng, Qingliang</creatorcontrib><creatorcontrib>Fan, Wei</creatorcontrib><creatorcontrib>Gu, Huimin</creatorcontrib><creatorcontrib>Cui, Jiakang</creatorcontrib><creatorcontrib>Wang, Huilian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Nan fang yi ke da xue xue bao = Journal of Southern Medical University</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhan, Junping</au><au>Huang, Shuo</au><au>Meng, Qingliang</au><au>Fan, Wei</au><au>Gu, Huimin</au><au>Cui, Jiakang</au><au>Wang, Huilian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Buyang Huanwu Decoction reduces mitochondrial autophagy in rheumatoid arthritis synovial fibroblasts in hypoxic culture by inhibiting the BNIP3-PI3K/Akt pathway</atitle><jtitle>Nan fang yi ke da xue xue bao = Journal of Southern Medical University</jtitle><addtitle>Nan Fang Yi Ke Da Xue Xue Bao</addtitle><date>2025-01-20</date><risdate>2025</risdate><volume>45</volume><issue>1</issue><spage>35</spage><pages>35-</pages><issn>1673-4254</issn><abstract>To investigate the role of the BNIP3-PI3K/Akt signaling pathway in mediating the inhibitory effect of
Decoction (BYHWT) on mitochondrial autophagy in human synovial fibroblasts from rheumatoid arthritis patients (FLS-RA) cultured under a hypoxic condition.
Forty normal Wistar rats were randomized into two groups (
=20) for daily gavage of BYHWT or distilled water for 7 days to prepare BYHWT-medicated or control sera. FLS-RA were cultured in routine condition or exposed to hypoxia (10% O
) for 24 h wigh subsequent treatment with IL-1β, followed by treatment with diluted BYHWT-medicated serum (5%, 10% and 20%) or control serum. AnnexinV-APC/7-AAD double staining and T-AOC kit were used for detecting apoptosis and total antioxidant capacity of the cells, and the changes in ROS, ATP level, mitochondrial membrane potential and Ca
homeostasis were analyzed. The changes in mRNA and protein expressions of BNIP3, PI3K and AKT and mRNA expressions of LC3, Beclin-1 and P62 were detected using RT-qPCR and Western blotting.
Treatment with BYHWT-medicated serum dose-dependently lowered apoptosis rate of IL-1β-induced FLS-RA with hypoxic exposure. The treatment significantly decreased T-AOC concentration, increased ROS production, autophagosome formation and ATPase levels, and lowered mitochondrial membrane potential and Ca
level in the cells. In IL-1β-induced FLS-RA with hypoxic exposure, treatment with BYHWT-medicated serum significantly increased BNIP3 protein expression, decreased the protein expressions of PI3K and AKT, increased the mRNA expressions of BNIP3 and P62, and lowered the mRNA expressions of PI3K, AKT, LC3 and Beclin-1 without significantly affecting Beclin-1 protein expression. The cells treated with 5% and 10% BYHWT-medicated serum showed no significant changes in LC3 expression.
BYHWT inhibits mitochondrial autophagy in IL-1β-induced FLS-RA with hypoxic exposure possibly by inhibiting BNIP3-mediated PI3K/AKT signaling pathway.</abstract><cop>China</cop><pmid>39819710</pmid><doi>10.12122/j.issn.1673-4254.2025.01.05</doi></addata></record> |
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| ispartof | Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025-01, Vol.45 (1), p.35 |
| issn | 1673-4254 |
| language | chi ; eng |
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| subjects | Animals Apoptosis - drug effects Arthritis, Rheumatoid - drug therapy Arthritis, Rheumatoid - metabolism Autophagy - drug effects Cells, Cultured Drugs, Chinese Herbal - pharmacology Fibroblasts - drug effects Fibroblasts - metabolism Humans Interleukin-1beta - metabolism Male Membrane Proteins - metabolism Mitochondria - drug effects Mitochondria - metabolism Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Wistar Signal Transduction - drug effects Synovial Membrane - cytology Synovial Membrane - drug effects Synovial Membrane - metabolism |
| title | Buyang Huanwu Decoction reduces mitochondrial autophagy in rheumatoid arthritis synovial fibroblasts in hypoxic culture by inhibiting the BNIP3-PI3K/Akt pathway |
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