Abstract

Fructus Ligustri Lucidi (FLL) is the fruit of Ligustrum lucidum Ait and is a component of many kidney-tonifying traditional Chinese medicine formulae for treating osteoporosis. Accumulating evidence has linked oxidative stress with the progression of bone diseases. The present study aimed to identify the effects of FLL on oxidative stress-related osteoporosis in vivo and in vitro. To construct animal models, we utilized d-galactose (D-gal) injection to induce oxidative stress combined with a low calcium (the exact percentage in the diet was 0.1%) diet. Thirteen-week-old Kunming female mice were gavaged with water extract of FLL for 20 days. Then, eight-month-old Kunming female mice were treated with FLL under standard administration and diet as the aged group. In vitro, MC3T3-E1 cells stimulated by H2O2 were treated with FLL for 24 h. The micro-CT results showed that the modeling approach combining oxidative stress with a low calcium diet caused low conversion type osteoporosis in mice. FLL exerted a prominent effect on preventing osteoporosis by inhibiting oxidative stress, increasing bone mineral density (BMD), improving bone microstructure, and promoting osteoblast proliferation and osteoprotegerin (OPG) protein expression; however, FLL had no therapeutic effect on bone loss in aged mice. In conclusion, FLL showed outstanding anti-bone loss ability both in vivo and in vitro and could probably be developed as a prophylactic agent for osteoporosis.

Highlights

  • Osteoporosis is a progressive asymptomatic bone disease characterized by a decrease in bone mass and mineral density, as well as a degeneration in the microstructure of bone tissue due to the depletion of calcium and bone protein [1]

  • Studies have shown that reactive oxygen species (ROS) produced by oxidative stress disrupted the balance between bone formation-related cells, such as bone marrow mesenchymal stem cells (BMSCs), osteoblasts, osteocytes. and osteoclasts [4,5]

  • ROS inhibits the differentiation of bone marrow stem cells into osteoblasts and promotes the differentiation of osteoclasts, all of which lead to decreased bone mass and bone strength and aggravate osteoporosis [6]

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Summary

Introduction

Osteoporosis is a progressive asymptomatic bone disease characterized by a decrease in bone mass and mineral density, as well as a degeneration in the microstructure of bone tissue due to the depletion of calcium and bone protein [1]. Oxidative stress theory has attracted increasing attention in osteoporosis research [2,3]. Studies have shown that reactive oxygen species (ROS) produced by oxidative stress disrupted the balance between bone formation-related cells, such as bone marrow mesenchymal stem cells (BMSCs), osteoblasts, osteocytes. ROS inhibits the differentiation of bone marrow stem cells into osteoblasts and promotes the differentiation of osteoclasts, all of which lead to decreased bone mass and bone strength and aggravate osteoporosis [6]. Accelerated aging by oxidative stress increases the intracellular calcium content and reduces the calcium transmembrane distribution gradient, thereby impairing the body’s ability to absorb calcium [7].

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