d-갈락토오스로 인한 쥐의 노화에 대한 코디세핀의 보호 효과: 심장에서 본 모습.

한국어 요약

2022년 발표된 「Protective effects of cordycepin against d-galactose-induced aging in rats: A view from the heart.」은(는) 균종 미특정 및 코디세핀 관련 동물·세포 실험(전임상)입니다. 아래는 원문 초록을 바탕으로 한 중립적 요약이며, 제품 효능·효과를 의미하지 않습니다.

초록 요지

AIMS: Aging is a critical contributing factor for cardiovascular diseases. The d-galactose-induced accelerated aging model is comparable to physiological aging from the cellular to the physiological level. The d-galactose treatment induces mitochondrial dysfunction, increased reactive oxygen species (ROS) production, and upregulation of senescence-related genes. Cordycepin, a functional element in Chinese traditional medicine, has multiple beneficial effects as an antioxidant and ROS scavenger, and has been reported to be effective in a number of ischemia models. This paper aims to investigate the cardioprotective effects of cordycepin in the d-galactose accelerated aging model. METHODS: In the current study, we employed the d-galactose accelerated aging model to study the cardioprotective effect of cordycepin. Eight-week-old Sprague-Dawley rats, randomly divided into five groups, were given vehicle, d-galactose (150 mg/kg/day), and cordycepin at 5, 10, and 20 mg/kg per day. At the end of the 8-week treatment, rat cardiac structure and function were assessed with echocardiographic imaging and hemodynamic parameter analysis. RESULTS: Cordycepin upregulated the expression of Klotho in serum and heart tissues. The expressions of senescence markers β-galactosidase, p21, and oxidative stress marker malondialdehyde (MDA) were downregulated by cordycepin treatment. Reduction of levels and activity of the antioxidant factors superoxide dismutase (SOD) and catalase (CAT) induced by by d-galactose treatment was ameliorated by cordycepin. Furthermore, cordycepin activated AMPK signaling in d-galactose-treated rats. After 8 weeks of treatment, we found that cordycepin improved myocardia contractility and hypertension caused by d-galactose treatment. Mechanistically, reduced expression of the Klotho protein SOD1 caused by d-galactose was recovered in rats co-treated with cordycepin. CONCLUSION: Cordycepin could protect against cardiac dysfunction in a d-galactose-induced aging rat model, suggesting the therapeutic cardioprotective potential of cordycepin in aging. Geriatr Gerontol Int 2022; 22: 433-440.

전문가 메모

• 연구 수준: 동물/세포 실험 · 동물·세포 실험(전임상)
• 대상: 균종 미특정 / cordycepin
• 제품 연관성: partial
• 해석 주의: 전임상(동물·세포) 결과는 인간 섭취·담금주 맥락으로 직접 확장하기 어렵습니다.
• 해석 주의: 원문에 질병·치료 관련 서술이 포함되어 있습니다. 본 요약은 성분·균류 연구 맥락만 중립적으로 정리했습니다.
• 인사이트: 배양·생산·기초 메커니즘 연구로 읽는 것이 적절합니다. 소비자 효능 주장 근거로 사용할 수 없습니다.

출처 · 원문

• 제목: Protective effects of cordycepin against d-galactose-induced aging in rats: A view from the heart.
• 저자: Yuanxi Feng, Qiang Huang
• 연도: 2022
• 저널: Geriatrics & gerontology international
• DOI: 10.1111/ggi.14376
• PMID: 35352454
• 링크: https://pubmed.ncbi.nlm.nih.gov/35352454/

원문 초록 (English)

Summary — AIMS: Aging is a critical contributing factor for cardiovascular diseases. The d-galactose-induced accelerated aging model is comparable to physiological aging from the cellular to the physiological level. The d-galactose treatment induces mitochondrial dysfunction, increased reactive oxygen species (ROS) production, and upregulation of senescence-related genes. Cordycepin, a functional element in Chinese traditional medicine, has multiple beneficial effects as an antioxidant and ROS scavenger, and has been reported to be effective in a number of ischemia models. This paper aims to investigate the cardioprotective effects of cordycepin in the d-galactose accelerated aging model. METHODS: In the current study, we employed the d-galactose accelerated aging model to study the cardioprotective effect of cordycepin. Eight-week-old Sprague-Dawley rats, randomly divided into five groups, were given vehicle, d-galactose (150 mg/kg/day), and cordycepin at 5, 10, and 20 mg/kg per day. At the end of the 8-week treatment, rat cardiac structure and function were assessed with echocardiographic imaging and hemodynamic parameter analysis. RESULTS: Cordycepin upregulated the expression of Klotho in serum and heart tissues. The expressions of senescence markers β-galactosidase, p21, and oxidative stress marker malondialdehyde (MDA) were downregulated by cordycepin treatment. Reduction of levels and activity of the antioxidant factors superoxide dismutase (SOD) and catalase (CAT) induced by by d-galactose treatment was ameliorated by cordycepin. Furthermore, cordycepin activated AMPK signaling in d-galactose-treated rats. After 8 weeks of treatment, we found that cordycepin improved myocardia contractility and hypertension caused by d-galactose treatment. Mechanistically, reduced expression of the Klotho protein SOD1 caused by d-galactose was recovered in rats co-treated with cordycepin. CONCLUSION: Cordycepin could protect against cardiac dysfunction in a d-galactose-induced aging rat model, suggesting the therapeutic cardioprotective potential of cordycepin in aging. Geriatr Gerontol Int 2022; 22: 433-440.

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