Abstract
In literature, antiosteoporotic effects of Angelica sinensis root have been confirmed, but the impact of Angelica sinensis polysaccharide (ASP) on osteoblastic or adipogenic distinction of BMSCs is limited. This paper aimed to explore the role of ASP on proliferation and differentiation of rat BMSCs. Rat BMSCs were subjected to isolation and identification through flow cytometry. The proliferation of rat BMSCs under ASP was performed by CCK-8 kit. Measures of osteogenesis under different concentrations of ASP were detected by using alizarin red staining for mesenchymal cells differentiation and ALP activity assay to identify ALP activity. Quantitative RT-PCR was selected to identify osteoblastic or adipogenic biomarkers from a genetic perspective. Likewise, we have evaluated measures of indicators of Wnt/β-catenin signal. ASP significantly promoted the proliferation, increased osteogenesis, and decreased adipogenesis of rat BMSCs within the limit of 20–60 mg/L in a dose-dependent manner but was suppressed at 80 mg/L. The expression of cyclin D1 and ß-catenin showed a considerable rise over the course of ASP induced osteogenesis. Dickkopf 1 (DKK1) suppressed the regulation of rat BMSCs differentiation through the mediation of ASP. We have observed that ASP upregulated the osteogenic but downregulated adipogenic differentiation of BMSCs, and our findings help to contribute to effective solutions for treating bone disorders.
Highlights
As the concentration of Angelica sinensis polysaccharide (ASP) rose from 20 mg/L to 60 mg/L, we found that measures of improvements of cell growth were more noticeable
Cell growth exhibited no improvement at a density of 80 mg/L, which suggested that ASP was conducive to the growth of rat bone marrow mesenchymal stem cells (BMSCs) in both a dose- and a time-dependent manner within the limits of 20–60 mg/L we assessed in our research approach
Directive e experiments, which were carried out during the proposed setup, have confirmed that ASP enhanced the proliferation of rat BMSCs by using dose-dependent methodology within the limit of 20–60 mg/L, whereas this impact was found to have been reduced at concentrations of 80 mg/L
Summary
Postmenopausal osteoporosis is one of the frequently reported skeletal disorders. is disorder has reportedly been considered one of the most crucial public health concerns of the ageing population. e main cause of postmenopausal osteoporosis is estrogen deficiency, this estrogen deficiency after menopause is linked with increased apoptosis of osteoblast (bone-forming cell) [1]. ese features can lead to increases in the possibility of both osteoclastogenesis and osteoclast, resulting in reduced weight of bone and elevated likelihood for osteoporosis [2].estrogen deficiency can cause increased proinflammatory cytokines production, contrasting the decrease in levels of bone-forming factors [3, 4]. is estrogen deficiency can create a more suitable environment for microbial proliferation and lead to an increased risk for infections of the oral cavity, which themselves may have a relationship with the varied bone condition of osteoporosis [5]. ese factors create a more prone environment for periimplantitis of osteoporosis patients, which acts as a major contributing component to success or failure for dental implantation in oral operations since it can decline formation of bone and negatively impact osseointegrationJournal of Healthcare Engineering around implants. E main cause of postmenopausal osteoporosis is estrogen deficiency, this estrogen deficiency after menopause is linked with increased apoptosis of osteoblast (bone-forming cell) [1]. Is estrogen deficiency can create a more suitable environment for microbial proliferation and lead to an increased risk for infections of the oral cavity, which themselves may have a relationship with the varied bone condition of osteoporosis [5]. Ese factors create a more prone environment for periimplantitis of osteoporosis patients, which acts as a major contributing component to success or failure for dental implantation in oral operations since it can decline formation of bone and negatively impact osseointegration. Erefore, a better understanding of the avoidance of implant loss by enhancing the success ratio for dental implants and of how to increase osseointegration in postmenopausal osteoporosis patients is urgently needed. AS extracts are postulated for possible in vitro inhibition of RANKL-affected osteoclast difference of bone marrow macrophages, which implies that AS has the potential to help prevent bone loss [15]
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