2. Academic Validation
  3. Carnosol attenuates angiotensin II-induced cardiac remodeling and inflammation via directly binding to p38 and inhibiting p38 activation

Carnosol attenuates angiotensin II-induced cardiac remodeling and inflammation via directly binding to p38 and inhibiting p38 activation

  • Int Immunopharmacol. 2024 Apr 30:134:112143. doi: 10.1016/j.intimp.2024.112143.
Diyun Xu 1,  Bozhi Ye 2,  Liming Lin 3,  Yanhong Jin 2,  Yuchen Jiang 3,  Zhaozheng Zheng 3,  Yanghao Chen 2,  Xue Han 4,  Wei Wang 5,  Gaojun Wu 6,  Zaishou Zhuang 7,  Peiren Shan 8,  Guang Liang 9
Affiliations

Affiliations

  • 1 The Affiliated Cangnan Hospital, Wenzhou Medical University, Wenzhou 325800, Zhejiang, China; Department of Cardiology and the Key Laboratory of Cardiovascular Disease of Wenzhou, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 2 Department of Cardiology and the Key Laboratory of Cardiovascular Disease of Wenzhou, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China; Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 3 Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 4 School of Pharmaceutical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China.
  • 5 Department of Neurosurgery, Affiliated Yongkang First People's Hospital, Hangzhou Medical College, Yongkang, Zhejiang 321399, China.
  • 6 Department of Cardiology and the Key Laboratory of Cardiovascular Disease of Wenzhou, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 7 The Affiliated Cangnan Hospital, Wenzhou Medical University, Wenzhou 325800, Zhejiang, China. Electronic address: zhuang372@163.com.
  • 8 Department of Cardiology and the Key Laboratory of Cardiovascular Disease of Wenzhou, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China. Electronic address: prshan@126.com.
  • 9 The Affiliated Cangnan Hospital, Wenzhou Medical University, Wenzhou 325800, Zhejiang, China; Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China; School of Pharmaceutical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China. Electronic address: wzmcliangguang@163.com.
PMID: 38692016 DOI: 10.1016/j.intimp.2024.112143
Abstract

Chronic inflammation is a significant contributor to hypertensive heart failure. Carnosol (Car), primarily derived from the sage plant (Salvia carnosa), exhibits anti-inflammatory properties in a range of systems. Nevertheless, the influence of angiotensin II (Ang II) on cardiac remodeling remains uncharted. Car was shown to protect mice's hearts against Ang II-induced heart damage at dosages of 20 and 40 mg/kg/d. This protection was evident in a concentration-related decrease in the remodeling of the heart and dysfunction. Examination of the transcriptome revealed that the pivotal roles in mediating the protective effects of Car involved inhibiting Ang II-induced inflammation and the activation of the mitogen-activated protein kinase (MAPK) pathway. Furthermore, Car was found to inhibit p38 phosphorylation, therefore reducing the level of inflammation in cultured cardiomyocytes and mouse hearts. This effect was attributed to the direct binding to p38 and inhibition of p38 protein phosphorylation by Car both in vitro and in vivo. In addition, the effects of Car on inflammation were neutralized when p38 was blocked in cardiomyocytes.

Keywords

Angiotensin II; Cardiac Remodeling; Carnosol; Inflammation; P38.

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