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  3. Chrysanthemum morifolium Extract Ameliorates Doxorubicin-Induced Cardiotoxicity by Decreasing Apoptosis

Chrysanthemum morifolium Extract Ameliorates Doxorubicin-Induced Cardiotoxicity by Decreasing Apoptosis

  • Cancers (Basel). 2022 Jan 28;14(3):683. doi: 10.3390/cancers14030683.
Masaya Ono 1,  Yoichi Sunagawa 1 2 3,  Saho Mochizuki 1,  Takahiro Katagiri 1,  Hidemichi Takai 1,  Sonoka Iwashimizu 1,  Kyoko Inai 1,  Masafumi Funamoto 1 2,  Kana Shimizu 1 2,  Satoshi Shimizu 1 2,  Yasufumi Katanasaka 1 2 3,  Maki Komiyama 2,  Philip Hawke 4,  Hideo Hara 5,  Yoshiki Arakawa 6,  Kiyoshi Mori 3 7 8,  Akira Asai 9,  Koji Hasegawa 1 2,  Tatsuya Morimoto 1 2 3
Affiliations

Affiliations

  • 1 Division of Molecular Medicine, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka 422-8526, Japan.
  • 2 Division of Translational Research, Clinical Research Institute, Kyoto Medical Center, National Hospital Organization, Kyoto 612-8555, Japan.
  • 3 Shizuoka General Hospital, Shizuoka 420-8527, Japan.
  • 4 Laboratory of Scientific English, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka 422-8526, Japan.
  • 5 UNIAL Co., Ltd., Tokyo 173-0005, Japan.
  • 6 Department of Neurosurgery, Kyoto University Graduate of Medicine, Kyoto 606-8507, Japan.
  • 7 Graduate School of Public Health, Shizuoka Graduate University of Public Health, Shizuoka 420-0881, Japan.
  • 8 Department of Molecular and Clinical Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka 422-8526, Japan.
  • 9 Center for Drug Discovery, Graduate School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka 422-8526, Japan.
PMID: 35158951 DOI: 10.3390/cancers14030683
Abstract

It is well known that the anthracycline Anticancer drug doxorubicin (DOX) induces cardiotoxicity. Recently, Chrysanthemum morifolium extract (CME), an extract of the purple chrysanthemum flower, has been reported to possess various physiological activities such as antioxidant and anti-inflammatory effects. However, its effect on DOX-induced cardiotoxicity is still unknown. An 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT)assay revealed that 1 mg/mL of CME reduced DOX-induced cytotoxicity in H9C2 cells but not in MDA-MB-231 cells. A TUNEL assay indicated that CME treatment improved DOX-induced Apoptosis in H9C2 cells. Moreover, DOX-induced increases in the expression levels of p53, phosphorylated p53, and cleaved Caspase-3,9 were significantly suppressed by CME treatment. Next, we investigated the effect of CME in vivo. The results showed that CME treatment substantially reversed the DOX-induced decrease in survival rate. Echocardiography indicated that CME treatment also reduced DOX-induced left ventricular systolic dysfunction, and a TUNEL assay showed that CME treatment also suppressed Apoptosis in the mouse heart. These results reveal that CME treatment ameliorated DOX-induced cardiotoxicity by suppressing Apoptosis. Further study is needed to clarify the effect of CME on DOX-induced heart failure in humans.

Keywords

Chrysanthemum morifolium; apoptosis; cardiomyopathy; doxorubicin; p53; systolic dysfunction.

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