Ginsenoside Rb1 and compound K improve insulin signaling and inhibit ER stress-associated NLRP3 inflammasome activation in adipose tissue
Background: This study was designed to investigate whether ginsenoside Rb1 (Rb1) and compound K (CK) ameliorated insulin resistance by suppressing endoplasmic reticulum (ER) stress-induced inflammation in adipose tissue. Methods: To induce ER stress, epididymal adipose tissue from mice or differenti...
| Main Authors: | , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2016-10-01
|
| Series: | Journal of Ginseng Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1226845315001098 |
| _version_ | 1818131224758059008 |
|---|---|
| author | Weijie Chen Junlian Wang Yong Luo Tao Wang Xiaochun Li Aiyun Li Jia Li Kang Liu Baolin Liu |
| author_facet | Weijie Chen Junlian Wang Yong Luo Tao Wang Xiaochun Li Aiyun Li Jia Li Kang Liu Baolin Liu |
| author_sort | Weijie Chen |
| collection | DOAJ |
| description | Background: This study was designed to investigate whether ginsenoside Rb1 (Rb1) and compound K (CK) ameliorated insulin resistance by suppressing endoplasmic reticulum (ER) stress-induced inflammation in adipose tissue.
Methods: To induce ER stress, epididymal adipose tissue from mice or differentiated 3T3 adipocytes were exposed to high glucose. The effects of Rb1 and CK on reactive oxygen species production, ER stress, TXNIP/NLRP3 inflammasome activation, inflammation, insulin signaling activation, and glucose uptake were detected by western blot, emzyme-linked immunosorbent assay, or fluorometry.
Results: Rb1 and CK suppressed ER stress by dephosphorylation of IRE1α and PERK, thereby reducing TXNIP-associated NLRP3 inflammasome activation in adipose tissue. As a result, Rb1 and CK inhibited IL-1β maturation and downstream inflammatory factor IL-6 secretion. Inflammatory molecules induced insulin resistance by upregulating phosphorylation of insulin receptor substrate-1 at serine residues and impairing insulin PI3K/Akt signaling, leading to decreased glucose uptake by adipocytes. Rb1 and CK reversed these changes by inhibiting ER stress-induced inflammation and ameliorating insulin resistance, thereby improving the insulin IRS-1/PI3K/Akt-signaling pathway in adipose tissue.
Conclusion: Rb1 and CK inhibited inflammation and improved insulin signaling in adipose tissue by suppressing ER stress-associated NLRP3 inflammation activation. These findings offered novel insight into the mechanism by which Rb1 and CK ameliorate insulin resistance in adipose tissue. |
| first_indexed | 2024-12-11T08:17:32Z |
| format | Article |
| id | doaj.art-700b8f834ddf46e7b19f1ad0c2bd8803 |
| institution | Directory Open Access Journal |
| issn | 1226-8453 |
| language | English |
| last_indexed | 2024-12-11T08:17:32Z |
| publishDate | 2016-10-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Ginseng Research |
| spelling | doaj.art-700b8f834ddf46e7b19f1ad0c2bd88032022-12-22T01:14:44ZengElsevierJournal of Ginseng Research1226-84532016-10-0140435135810.1016/j.jgr.2015.11.002Ginsenoside Rb1 and compound K improve insulin signaling and inhibit ER stress-associated NLRP3 inflammasome activation in adipose tissueWeijie ChenJunlian WangYong LuoTao WangXiaochun LiAiyun LiJia LiKang LiuBaolin LiuBackground: This study was designed to investigate whether ginsenoside Rb1 (Rb1) and compound K (CK) ameliorated insulin resistance by suppressing endoplasmic reticulum (ER) stress-induced inflammation in adipose tissue. Methods: To induce ER stress, epididymal adipose tissue from mice or differentiated 3T3 adipocytes were exposed to high glucose. The effects of Rb1 and CK on reactive oxygen species production, ER stress, TXNIP/NLRP3 inflammasome activation, inflammation, insulin signaling activation, and glucose uptake were detected by western blot, emzyme-linked immunosorbent assay, or fluorometry. Results: Rb1 and CK suppressed ER stress by dephosphorylation of IRE1α and PERK, thereby reducing TXNIP-associated NLRP3 inflammasome activation in adipose tissue. As a result, Rb1 and CK inhibited IL-1β maturation and downstream inflammatory factor IL-6 secretion. Inflammatory molecules induced insulin resistance by upregulating phosphorylation of insulin receptor substrate-1 at serine residues and impairing insulin PI3K/Akt signaling, leading to decreased glucose uptake by adipocytes. Rb1 and CK reversed these changes by inhibiting ER stress-induced inflammation and ameliorating insulin resistance, thereby improving the insulin IRS-1/PI3K/Akt-signaling pathway in adipose tissue. Conclusion: Rb1 and CK inhibited inflammation and improved insulin signaling in adipose tissue by suppressing ER stress-associated NLRP3 inflammation activation. These findings offered novel insight into the mechanism by which Rb1 and CK ameliorate insulin resistance in adipose tissue.http://www.sciencedirect.com/science/article/pii/S1226845315001098compound kendoplasmic reticulum stressginsenoside Rb1insulin resistanceNLRP3 inflammasome |
| spellingShingle | Weijie Chen Junlian Wang Yong Luo Tao Wang Xiaochun Li Aiyun Li Jia Li Kang Liu Baolin Liu Ginsenoside Rb1 and compound K improve insulin signaling and inhibit ER stress-associated NLRP3 inflammasome activation in adipose tissue Journal of Ginseng Research compound k endoplasmic reticulum stress ginsenoside Rb1 insulin resistance NLRP3 inflammasome |
| title | Ginsenoside Rb1 and compound K improve insulin signaling and inhibit ER stress-associated NLRP3 inflammasome activation in adipose tissue |
| title_full | Ginsenoside Rb1 and compound K improve insulin signaling and inhibit ER stress-associated NLRP3 inflammasome activation in adipose tissue |
| title_fullStr | Ginsenoside Rb1 and compound K improve insulin signaling and inhibit ER stress-associated NLRP3 inflammasome activation in adipose tissue |
| title_full_unstemmed | Ginsenoside Rb1 and compound K improve insulin signaling and inhibit ER stress-associated NLRP3 inflammasome activation in adipose tissue |
| title_short | Ginsenoside Rb1 and compound K improve insulin signaling and inhibit ER stress-associated NLRP3 inflammasome activation in adipose tissue |
| title_sort | ginsenoside rb1 and compound k improve insulin signaling and inhibit er stress associated nlrp3 inflammasome activation in adipose tissue |
| topic | compound k endoplasmic reticulum stress ginsenoside Rb1 insulin resistance NLRP3 inflammasome |
| url | http://www.sciencedirect.com/science/article/pii/S1226845315001098 |
| work_keys_str_mv | AT weijiechen ginsenosiderb1andcompoundkimproveinsulinsignalingandinhibiterstressassociatednlrp3inflammasomeactivationinadiposetissue AT junlianwang ginsenosiderb1andcompoundkimproveinsulinsignalingandinhibiterstressassociatednlrp3inflammasomeactivationinadiposetissue AT yongluo ginsenosiderb1andcompoundkimproveinsulinsignalingandinhibiterstressassociatednlrp3inflammasomeactivationinadiposetissue AT taowang ginsenosiderb1andcompoundkimproveinsulinsignalingandinhibiterstressassociatednlrp3inflammasomeactivationinadiposetissue AT xiaochunli ginsenosiderb1andcompoundkimproveinsulinsignalingandinhibiterstressassociatednlrp3inflammasomeactivationinadiposetissue AT aiyunli ginsenosiderb1andcompoundkimproveinsulinsignalingandinhibiterstressassociatednlrp3inflammasomeactivationinadiposetissue AT jiali ginsenosiderb1andcompoundkimproveinsulinsignalingandinhibiterstressassociatednlrp3inflammasomeactivationinadiposetissue AT kangliu ginsenosiderb1andcompoundkimproveinsulinsignalingandinhibiterstressassociatednlrp3inflammasomeactivationinadiposetissue AT baolinliu ginsenosiderb1andcompoundkimproveinsulinsignalingandinhibiterstressassociatednlrp3inflammasomeactivationinadiposetissue |