학술논문
Cardioprotection via mitochondrial transplantation supports fatty acid metabolism in ischemia-reperfusion injured rat heart
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- 영문명
- 발행기관
- 대한생리학회-대한약리학회
- 저자명
- Jehee Jang Ki-Woon Kang Young-Won Kim Seohyun Jeong Jaeyoon Park Jihoon Park Jisung Moon Junghyun Jang Seohyeon Kim Sunghun Kim Sungjoo Cho Yurim Lee Hyoung Kyu Kim Jin Han Eun-A Ko Sung-Cherl Jung Jung-Ha Kim Jae-Hong Ko
- 간행물 정보
- 『The Korean Journal of Physiology & Pharmacology』제28권 제3호, 209~217쪽, 전체 9쪽
- 주제분류
- 의약학 > 의학일반
- 파일형태
- 발행일자
- 2024.05.01
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국문 초록
In addition to cellular damage, ischemia-reperfusion (IR) injury induces substantial damage to the mitochondria and endoplasmic reticulum. In this study, we sought to determine whether impaired mitochondrial function owing to IR could be restored by transplanting mitochondria into the heart under ex vivo IR states. Ad-ditionally, we aimed to provide preliminary results to inform therapeutic options for ischemic heart disease (IHD). Healthy mitochondria isolated from autologous gluteus maximus muscle were transplanted into the hearts of Sprague–Dawley rats dam-aged by IR using the Langendorff system, and the heart rate and oxygen consump-tion capacity of the mitochondria were measured to confirm whether heart function was restored. In addition, relative expression levels were measured to identify the genes related to IR injury. Mitochondrial oxygen consumption capacity was found to be lower in the IR group than in the group that underwent mitochondrial transplan-tation after IR injury (p < 0.05), and the control group showed a tendency toward increased oxygen consumption capacity compared with the IR group. Among the genes related to fatty acid metabolism, Cpt1b (p < 0.05) and Fads1 (p < 0.01) showed significant expression in the following order: IR group, IR + transplantation group, and control group. These results suggest that mitochondrial transplantation protects the heart from IR damage and may be feasible as a therapeutic option for IHD.
영문 초록
목차
INTRODUCTION
METHODS
RESULTS
DISCUSSION
키워드
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