Oral Administration of Quercetin or Its Derivatives Inhibit Bone Loss in Animal Model of Osteoporosis

Abstract

Objectives. Quercetin (Q) and its derivatives are the major members of the naturally occurring flavonoid family, which possess beneficial effects on disease prevention including osteoporosis. The present study is aimed at further investigating the efficacy of the Q and its derivatives on bone pathology, bone-related parameters under imageology, bone maximum load, and serum bone metabolism indexes in animal model of osteoporosis. Potential mechanisms of Q and its derivatives in the treatment of osteoporosis as well as the existing problems regarding the modeling method and limitations of researches in this area were also summarized. Eight databases were searched from their inception dates to February 2020. Nineteen eligible studies containing 21 comparisons were identified ultimately. The risk of bias and data on outcome measures were analyzed by the CAMARADES 10-item checklist and Rev-Man 5.3 software separately. The results displayed the number of criteria met varied from 3/10 to 7/10 with an average of 5.05. The present study provided the preliminary preclinical evidence that oral administration of Q or its derivatives was capable of improving bone pathology, bone-related parameters under imageology and bone maximum load, increasing serum osteocalcin, alkaline phosphatase, and estradiol, and reducing serum c-terminal cross-linked telopeptide of type I collagen (P < 0.05). No statistical difference was seen in survival rate, index of liver, or kidney function (P > 0.05). Q and its derivatives partially reverse osteopenia probably via antioxidant, anti-inflammatory, promoting osteogenesis, inhibiting osteoclasts, and its estrogen-like effect. The findings reveal the possibility of developing Q or its derivatives as a drug or an ingredient in diet for clinical treatment of osteoporosis.

Figure 1

The chemical structure of Q and its derivatives.

Figure 2

Summary of the process for identifying candidate studies.

Figure 3

The forest plot: effects of Q or its derivatives for increasing L-BMD compared with the control group.

Figure 4

The forest plot: effects of Q or its derivatives for increasing F-BMD compared with the control group.

Figure 5

(a) The forest plot: effects of Q or its derivatives for increasing Tb.Th compared with the control group; (b) The forest plot: effects of Q or its derivatives for increasing Tb.N compared with the control group.

Figure 6

The forest plot: effects of Q or its derivatives for increasing bone maximum load compared with the control group.

Figure 7

The forest plot: effects of Q or its derivatives for increasing serum estradiol level compared with the control group.

Figure 8

The forest plot: effects of Q or its derivatives for increasing uterine weight of experimental animals compared with the control group.

Figure 9

The forest plot: effects of Q or its derivatives on the survival rate of experimental animals compared with the control group.

Figure 10

Subgroup analyses of the F-BMD. (a) The different effect size between the ovariectomized model group and nonovariectomized model group; (b) the different effect size between mice and rats; (c) the different effect size between Q and its derivatives; (d) the different effect size between different treatment time group. ^#P < 0.05 vs. control groups; ^∗P > 0.05 vs. control groups.

Figure 11

A schematic representation of osteoprotective mechanisms of Q and its derivatives for osteoporosis.