Oridonin Relieves Angiotensin II-Induced Cardiac Remodeling via Inhibiting GSDMD-Mediated Inflammation
Myocardial remodeling is one of the main lesions in the late stage of chronic heart failure and seriously affects the prognosis of patients. Continuous activation of the renin-angiotensin-aldosterone system (RAAS) contributes to the development of myocardial remodeling greatly, and angiotensin II (A...
Saved in:
| Main Authors: | , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2022-01-01
|
| Series: | Cardiovascular Therapeutics |
| Online Access: | http://dx.doi.org/10.1155/2022/3167959 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832564893516038144 |
|---|---|
| author | Shuang Lin Shanshan Dai Jiahui Lin Xiaohe Liang Weiqi Wang Weijian Huang Bozhi Ye Xia Hong |
| author_facet | Shuang Lin Shanshan Dai Jiahui Lin Xiaohe Liang Weiqi Wang Weijian Huang Bozhi Ye Xia Hong |
| author_sort | Shuang Lin |
| collection | DOAJ |
| description | Myocardial remodeling is one of the main lesions in the late stage of chronic heart failure and seriously affects the prognosis of patients. Continuous activation of the renin-angiotensin-aldosterone system (RAAS) contributes to the development of myocardial remodeling greatly, and angiotensin II (Ang II), its main constituent, can directly lead to cardiac remodeling through an inflammatory response and oxidative stress. Since Ang II-induced myocardial remodeling is closely related to inflammation, we tried to explore whether the anti-inflammatory drug oridonin (Ori) can reverse this process and its possible mechanism. Our study investigated that hypertrophy and fibrosis can be induced after being treated with Ang II in cardiomyocytes (H9c2 cells and primary rat cardiomyocytes) and C57BL/6J mice. The anti-inflammatory drug oridonin could effectively attenuate the degree of cardiac remodeling both in vivo and vitro by inhibiting GSDMD, a key protein of intracellular inflammation which can further activate kinds of inflammation factors such as IL-1β and IL-18. We illustrated that oridonin reversed cardiac remodeling by inhibiting the process of inflammatory signaling through GSDMD. After inhibiting the expression of GSDMD in cardiomyocytes by siRNA, it was found that Ang II-induced hypertrophy was attenuated. These results suggest that oridonin is proved to be a potential protective drug against GSDMD-mediated inflammation and myocardial remodeling. |
| format | Article |
| id | doaj-art-7928f342d8744c7689ee44b07c01c312 |
| institution | Kabale University |
| issn | 1755-5922 |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Cardiovascular Therapeutics |
| spelling | doaj-art-7928f342d8744c7689ee44b07c01c3122025-02-03T01:09:54ZengWileyCardiovascular Therapeutics1755-59222022-01-01202210.1155/2022/3167959Oridonin Relieves Angiotensin II-Induced Cardiac Remodeling via Inhibiting GSDMD-Mediated InflammationShuang Lin0Shanshan Dai1Jiahui Lin2Xiaohe Liang3Weiqi Wang4Weijian Huang5Bozhi Ye6Xia Hong7The Key Laboratory of Cardiovascular Disease of WenzhouDepartment of EmergencyWenzhou Medical UniversityThe Key Laboratory of Cardiovascular Disease of WenzhouThe Key Laboratory of Cardiovascular Disease of WenzhouThe Key Laboratory of Cardiovascular Disease of WenzhouThe Key Laboratory of Cardiovascular Disease of WenzhouThe Key Laboratory of Cardiovascular Disease of WenzhouMyocardial remodeling is one of the main lesions in the late stage of chronic heart failure and seriously affects the prognosis of patients. Continuous activation of the renin-angiotensin-aldosterone system (RAAS) contributes to the development of myocardial remodeling greatly, and angiotensin II (Ang II), its main constituent, can directly lead to cardiac remodeling through an inflammatory response and oxidative stress. Since Ang II-induced myocardial remodeling is closely related to inflammation, we tried to explore whether the anti-inflammatory drug oridonin (Ori) can reverse this process and its possible mechanism. Our study investigated that hypertrophy and fibrosis can be induced after being treated with Ang II in cardiomyocytes (H9c2 cells and primary rat cardiomyocytes) and C57BL/6J mice. The anti-inflammatory drug oridonin could effectively attenuate the degree of cardiac remodeling both in vivo and vitro by inhibiting GSDMD, a key protein of intracellular inflammation which can further activate kinds of inflammation factors such as IL-1β and IL-18. We illustrated that oridonin reversed cardiac remodeling by inhibiting the process of inflammatory signaling through GSDMD. After inhibiting the expression of GSDMD in cardiomyocytes by siRNA, it was found that Ang II-induced hypertrophy was attenuated. These results suggest that oridonin is proved to be a potential protective drug against GSDMD-mediated inflammation and myocardial remodeling.http://dx.doi.org/10.1155/2022/3167959 |
| spellingShingle | Shuang Lin Shanshan Dai Jiahui Lin Xiaohe Liang Weiqi Wang Weijian Huang Bozhi Ye Xia Hong Oridonin Relieves Angiotensin II-Induced Cardiac Remodeling via Inhibiting GSDMD-Mediated Inflammation Cardiovascular Therapeutics |
| title | Oridonin Relieves Angiotensin II-Induced Cardiac Remodeling via Inhibiting GSDMD-Mediated Inflammation |
| title_full | Oridonin Relieves Angiotensin II-Induced Cardiac Remodeling via Inhibiting GSDMD-Mediated Inflammation |
| title_fullStr | Oridonin Relieves Angiotensin II-Induced Cardiac Remodeling via Inhibiting GSDMD-Mediated Inflammation |
| title_full_unstemmed | Oridonin Relieves Angiotensin II-Induced Cardiac Remodeling via Inhibiting GSDMD-Mediated Inflammation |
| title_short | Oridonin Relieves Angiotensin II-Induced Cardiac Remodeling via Inhibiting GSDMD-Mediated Inflammation |
| title_sort | oridonin relieves angiotensin ii induced cardiac remodeling via inhibiting gsdmd mediated inflammation |
| url | http://dx.doi.org/10.1155/2022/3167959 |
| work_keys_str_mv | AT shuanglin oridoninrelievesangiotensiniiinducedcardiacremodelingviainhibitinggsdmdmediatedinflammation AT shanshandai oridoninrelievesangiotensiniiinducedcardiacremodelingviainhibitinggsdmdmediatedinflammation AT jiahuilin oridoninrelievesangiotensiniiinducedcardiacremodelingviainhibitinggsdmdmediatedinflammation AT xiaoheliang oridoninrelievesangiotensiniiinducedcardiacremodelingviainhibitinggsdmdmediatedinflammation AT weiqiwang oridoninrelievesangiotensiniiinducedcardiacremodelingviainhibitinggsdmdmediatedinflammation AT weijianhuang oridoninrelievesangiotensiniiinducedcardiacremodelingviainhibitinggsdmdmediatedinflammation AT bozhiye oridoninrelievesangiotensiniiinducedcardiacremodelingviainhibitinggsdmdmediatedinflammation AT xiahong oridoninrelievesangiotensiniiinducedcardiacremodelingviainhibitinggsdmdmediatedinflammation |