Shengu'an exerts anti-osteoporotic effect in rats via TGFβ1-Smad2/3 signal pathway, and enhancement of bone and cartilage metabolism

Purpose: To study the anti-osteoporotic effect of Shengu'an in rats, and elucidate the mechanism of action involved.Methods: Forty healthy female SPF mice were randomly divided into control group, saline-treated group, TGFβRⅡ receptor inhibitor group, and shengu'an group. The expressions o...

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Veröffentlicht in:Tropical journal of pharmaceutical research 2020-11, Vol.19 (6), p.1191-1196
Hauptverfasser: Li, Wei, Peng, Zhiqiang, Wu, Yulun, Hu, Jintao, Li, Peilun, Yao, Xinmiao
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Sprache:eng
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Zusammenfassung:Purpose: To study the anti-osteoporotic effect of Shengu'an in rats, and elucidate the mechanism of action involved.Methods: Forty healthy female SPF mice were randomly divided into control group, saline-treated group, TGFβRⅡ receptor inhibitor group, and shengu'an group. The expressions of type Ⅱ collagen (Co1-II) and platelet endothelial cell adhesion factor (CD-31) were determined. The expressions of transforming growth factor β1 (TGF-β1), p-smad2/3, matrix metalloproteinase-9 (MMP-9) and osteoblast specific transcription factor (osterix) were assayed by western blotting.Results: The expression of Co1-II in the vertebral body was significantly lower in model mice than in control mice, but was significantly higher in shengu'an mice when compared with model mice (p < 0.05). In shengu'an mice, CoI-I was markedly upregulated, relative to model mice, and the expressions of CD31 in TGFβRⅡreceptor inhibitor group and shengu'an group were lower than in model group (p < 0.05). There were significantly lower expressions of TGF-β1 and p-smad2/3 in the vertebral body of shengu'an group than in model mice, but osterix was upregulated relative to model mice (p < 0.05).Conclusion: Shengu'an exerts anti-osteoporotic effect by downregulating TGFβ/smad signal pathway. There is thus a potential for its clinical application in the management of osteoporosis. Keywords: Shengu'an, TGFβ1-Smad2/3 signal, Bone cartilage metabolism, Osteoporosis
ISSN:1596-5996
1596-9827
DOI:10.4314/tjpr.v19i6.11