scholarly journals Exploring the Effect of Jiawei Buguzhi Pills on TGF-β-Smad Pathway in Postmenopausal Osteoporosis Based on Integrated Pharmacological Strategy

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Xiao Yuan ◽  
Yonghe Wu ◽  
Kailin Yang ◽  
Huiping Liu ◽  
Guomin Zhang

Objective. To explore the effect of Jiawei Buguzhi Pills (JWBGZP) on the TGF-β-Smad pathway in postmenopausal osteoporosis (PMO) based on integrated pharmacological strategy. Method. The ETCM database was used to collect JWBGZP. GeneCards and OMIM databases were utilized to obtain PMO-related genes. Cytoscape was used for network construction and analysis, and DAVID was used for GO and KEGG enrichment analysis of key targets. Animal experiments and cell experiments were conducted to further explore the mechanism. The bone mass density was detected by dual-energy X-ray bone densitometer. The TGF-β1 and Smad4 mRNA in bone tissue were detected by RT-qPCR. The TGF-β1 and Smad4 protein in bone tissue were detected by the western blot. The TGF-β1 and Smad4 protein in osteoblasts were determined by immunohistochemistry. Result. A total of 721 JWBGZP potential targets and 385 PMO-related genes were obtained. The enrichment analysis showed that JWBGZP may regulate the TGF-beta signaling pathway, oxidation-reduction process, aging, response to hypoxia, response to ethanol, negative regulation of cell proliferation, PI3K-Akt, HIF-1, and other signaling pathways. The animal experiments showed that compared with the model group, the femoral bone mineral density and lumbar bone mineral density of the JWBGZP group increased (P < 0.05); the expression levels of TGF-β1 and Smad mRNA and proteins in the JWBGZP group were significantly higher (P < 0.05). The cell experiment results showed a large number of osteoblast stained blue-purple and orange-red calcified nodules. The expression levels of TGF-β1 and Smad proteins in the JWBGZP group were significantly higher than those in the blank control group and the sham operation group, and the protein expression levels in the model group were the lowest (P < 0.05). Conclusion. JWBGZP may be involved in PI3K-Akt, HIF-1, estrogen, prolactin, and other signaling pathways and regulate MAPK1, AKT1, PIK3CA, JAK2, and other gene targets, regulate bone metabolism, and thereby treat PMO.

Author(s):  
Asma Al Salmani ◽  
Asma Al Shidhani ◽  
Nouf M Al-Alawi ◽  
Arwa A Al Sulaimi ◽  
Maha A Al-Hashemi

Objectives: Postmenopausal osteoporosis is a progressive metabolic bone disease resulting from estrogen deficiency. However, due to the silent nature of the disease, there is an urgent need for a simple, early predictive marker. This study, conducted between January 2017 to December 2019, aimed to assess the potential of three factors—specifically, the neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and platelet-to-lymphocyte ratio (PLR)—as inflammatory markers of bone mineral density (BMD) loss. Methods: A retrospective cross-sectional study was conducted among 450 postmenopausal Omani women undergoing dual-energy X-ray absorptiometry at the Sultan Qaboos University Hospital, Muscat, Oman. Participants were allocated into groups based on lumbar spine BMD t-score values. A receiver-operating characteristic curve was used to find the area under the curve (AUC). Multivariate logistic regression was performed to identify independent predictors of low BMD. Results: A total of 65 (14.4%), 164 (36.4%), and 221 (49.1%) women were allocated to the control, osteopenia, and osteoporosis groups, respectively. No significant differences in PLR, MLR, and NLR values were observed based on group allocation. BMD t-score values were reversely correlated with age (P = 0.007) and PLR (P = 0.004), and positively correlated with body mass index (BMI) (P <0.001). The AUC was 0.59. However, the only independent predictors of low BMD were age (>65 years) and BMI (<25 kg/m2). Conclusion: None of the three inflammatory biomarkers studied were found to be useful prognostic indicators of bone loss. Further research is recommended to reject or support theories regarding the role of inflammatory status in the pathogenesis. Keywords: inflammatory markers, neutrophil-to-lymphocyte ratio, monocyte-to-lymphocyte ratio, platelet-to-lymphocyte ratio, Bone mineral density, osteoporosis


2020 ◽  
Vol 19 (4) ◽  
pp. 811-815
Author(s):  
Maoxiu Peng ◽  
Gangyl Jiang ◽  
Shaoqi He ◽  
Chengxuan Tang

Purpose: To investigate the effect of ginsenoside Rg3 on bone loss, bone mineral density (BMD) and osteoclast number in glucocorticoid-induced osteoporosis (GIOP) rats, and the mechanism of action involved.Methods: Sixty female Wistar rats were assigned to control, model group, ginsenoside Rg3, and alendronate sodium groups, comprised of 15 rats per group. The osteoporosis rat model was established via intramuscular injection of dexamethasone. Changes in bone mineral content (BMC), BMD trabecular thickness and area, osteoblasts and osteoclasts in femurs and lumbar vertebrae were measured after 3 months of treatment.Results: There were significantly higher BMC and BMD levels in ginsenoside Rg3 group than in alendronate rats (p < 0.05). The thickness and  trabecular area in femur and lumbar vertebrae in the ginsenoside Rg3 group were significantly higher than those in the model group (p < 0.05), but were comparable with those in the alendronate sodium group (p > 0.05). There were marked increases in osteoblasts, and marked decreases in osteoclasts in the ginsenoside Rg3 group, alendronate sodium and control rats, relative to model rats (p < 0.05).Conclusion: Ginsenoside Rg3 arrests bone loss, and enhances bone density, trabecular thickness and area, bone microstructure, osteoblast activity and population of osteoclasts number in glucocorticoidinduced osteoporotic rats. This provides a new research direction for the clinical treatment ofosteoporosis. Keywords: Ginseng soap, Rg3, Glucocorticoid, Osteoporosis, Bone loss, Bone mineral density, Osteoclast population


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