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<p>Diabetic cardiomyopathy (DCM) is the leading cause of death in diabetic complications. Inflammation and oxidative stress greatly influence the progression of DCM and there are limited therapeutic opportunities. It has been shown that camel whey protein (CWP), a functional dairy ingredient has antioxidant and anti-inflammatory properties. Our objective is to illustrate the cardioprotective effect of CWP, a natural product in DCM and underlying mechanism of action. We found in type Ⅰ diabetic mice induced by STZ, oral intake of CWP significantly prevents cardiac hypertrophy. The biomarkers of inflammation, oxidative stress and cell apoptosis in heart tissue were also suppressed by CWP. Further, we determined the activation of antioxidant nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in regulating this molecular niche. By using neonatal rat ventricular myocytes (NRVMs) treated with high glucose, we found that CWP protects cells from oxidative stress and cell apoptosis. Our results suggested that CWP could serve as a clinical nutritional supplement in the prevention of DCM due to its function of suppressing inflammation, oxidative stress and cell apoptosis.</p>

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Camel Whey protein ameliorates type Ⅰ diabetic cardiomyopathy by mitigating oxidative stress, inflammation and apoptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月11日

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  • Zeyan Peng,
  • Jingyang Wang,
  • Zhili He,
  • Ziwei Chen,
  • Han Wei,
  • Xiaowen Zhang,
  • Zhiyong Shi,
  • Zhiyong Wang,
  • Liang Yang,
  • Jie Yan,
  • Jing Li,
  • Jianlin Cui,
  • LiFeng Feng,
  • Ying Liu,
  • HaiTao Yue,
  • Kai-Chiang YANG,
  • Zhi Qi,
  • Jie Yang,
  • Yang Gao

摘要

Diabetic cardiomyopathy (DCM) is the leading cause of death in diabetic complications. Inflammation and oxidative stress greatly influence the progression of DCM and there are limited therapeutic opportunities. It has been shown that camel whey protein (CWP), a functional dairy ingredient has antioxidant and anti-inflammatory properties. Our objective is to illustrate the cardioprotective effect of CWP, a natural product in DCM and underlying mechanism of action. We found in type Ⅰ diabetic mice induced by STZ, oral intake of CWP significantly prevents cardiac hypertrophy. The biomarkers of inflammation, oxidative stress and cell apoptosis in heart tissue were also suppressed by CWP. Further, we determined the activation of antioxidant nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in regulating this molecular niche. By using neonatal rat ventricular myocytes (NRVMs) treated with high glucose, we found that CWP protects cells from oxidative stress and cell apoptosis. Our results suggested that CWP could serve as a clinical nutritional supplement in the prevention of DCM due to its function of suppressing inflammation, oxidative stress and cell apoptosis.