2. Academic Validation
  3. Cinnamaldehyde Alleviates Bone Loss by Targeting Oxidative Stress and Mitochondrial Damage via the Nrf2/HO-1 Pathway in BMSCs and Ovariectomized Mice

Cinnamaldehyde Alleviates Bone Loss by Targeting Oxidative Stress and Mitochondrial Damage via the Nrf2/HO-1 Pathway in BMSCs and Ovariectomized Mice

  • J Agric Food Chem. 2023 Nov 2. doi: 10.1021/acs.jafc.3c03501.
Bing-Hao Lin 1 2,  Run-Xun Ma 1 2,  Jing-Tao Wu 1 2,  Shi-Qi Du 2 3,  Yi-Yun Lv 2 3,  Hao-Nan Yu 2 3,  Wei Zhang 1 2,  Shu-Ming Mao 1 2,  Guang-Yao Liu 1 2,  Yi-Tian Bu 1 2,  Zi-Hao Chen 1 2,  Chen Jin 1 2,  Zong-Yi Wu 1 2,  Lei Yang 1 2
Affiliations

Affiliations

  • 1 Department of Orthopedic, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325000, China.
  • 2 Key Laboratory of Orthopedics of Zhejiang Province, Wenzhou 325000, China.
  • 3 Wenzhou Medical University, Wenzhou 325000, China.
PMID: 37917162 DOI: 10.1021/acs.jafc.3c03501
Abstract

Osteoporosis (OP) is typically brought on by disruption of bone homeostasis. Excessive oxidative stress and mitochondrial dysfunction are believed to be the primary mechanisms underlying this disorder. Therefore, in order to restore bone homeostasis effectively, targeted treatment of oxidative stress and mitochondrial dysfunction is necessary. Cinnamaldehyde (CIN), a small molecule that acts as an agonist for the nuclear factor erythroid 2-related factor (Nrf2), has been found to possess antiapoptotic, anti-inflammatory, and antioxidant properties. We found that CIN, while rescuing Apoptosis, can also reduce the accumulation of Reactive Oxygen Species (ROS) to improve mitochondrial dysfunction and thus restore the osteogenic differentiation potential of BMSCs disrupted by hydrogen peroxide (H2O2) exposure. The role of CIN was preliminarily considered to be a consequence of Nrf2/HO-1 axis activation. The ovariectomized mice model further demonstrated that CIN treatment ameliorated oxidative stress in vivo, partially reversing OVX-induced bone loss. This improvement was seen in the trabecular microarchitecture and bone biochemical indices. However, when ML385 was concurrently injected with CIN, the positive effects of CIN were largely blocked. In conclusion, this study sheds LIGHT on the intrinsic mechanisms by which CIN regulates BMSCs and highlights the potential therapeutic applications of these findings in the treatment of osteoporosis.

Keywords

Nrf2/HO-1 pathway; bone marrow mesenchymal stem cells; cinnamaldehyde; mitochondrial dysfunction; reactive oxygen species.

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