Lycopene Promotes Osteogenesis and Reduces Adipogenesis through Regulating FoxO1/PPARγ Signaling in Ovariectomized Rats and Bone Marrow Mesenchymal Stem Cells

Author:

Xia Bingke1,Dai Xuan1,Shi Hanfen1,Yin Jiyuan1,Xu Tianshu1,Liu Tianyuan1,Yue Gaiyue1,Guo Haochen1,Liang Ruiqiong1,Liu Yage12,Gao Junfeng3,Wang Xinxiang3,Chen Xiaofei4,Tang Jinfa4,Wang Lili5,Zhu Ruyuan6ORCID,Zhang Dongwei1ORCID

Affiliation:

1. Diabetes Research Center, Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029, China

2. Food and Pharmacy College, Xuchang University, 88 Bayi Road, Xuchang 461000, China

3. The Scientific Research Center, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing 100078, China

4. Department of Pharmacology, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450003, China

5. Department of TCM Pharmacology, Chinese Material Medica School, Beijing University of Chinese Medicine, Beijing 102488, China

6. Institute of Basic Theory for Chinese Medicine, China Academy of Chinese Medical Sciences, Beijing 100700, China

Abstract

Recent interest in preventing the development of osteoporosis has focused on the regulation of redox homeostasis. However, the action of lycopene (LYC), a strong natural antioxidant compound, on osteoporotic bone loss remains largely unknown. Here, we show that oral administration of LYC to OVX rats for 12 weeks reduced body weight gain, improved lipid metabolism, and preserved bone quality. In addition, LYC treatment inhibited ROS overgeneration in serum and bone marrow in OVX rats, and in BMSCs upon H2O2 stimulation, leading to inhibiting adipogenesis and promoting osteogenesis during bone remodeling. At the molecular level, LYC improved bone quality via an increase in the expressions of FoxO1 and Runx2 and a decrease in the expressions of PPARγ and C/EBPα in OVX rats and BMSCs. Collectively, these findings suggest that LYC attenuates osteoporotic bone loss through promoting osteogenesis and inhibiting adipogenesis via regulation of the FoxO1/PPARγ pathway driven by oxidative stress, presenting a novel strategy for osteoporosis management.

Funder

National Natural Science Foundation of China

Fundamental Research Funds for the Central Public Welfare Research Institutes

Publisher

MDPI AG

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