• The Korea Journal of Herbology
• /
• v.38 no.4
• /
• pp.31-43
• /
• 2023

Objectives : The objective of this study was to investigate the phytochemistry and pharmacological activities of Cirsium setidens. Methods : Domestic and international articles about Cirsium setidens were investigated. A review was perfoemed via DB searching engine such as Sci.Direct, Springer, DBpia, KISS, Google scholar, Kipris, and so on. Total 73 listed literature were classified by compound analysis and pharmacological efficacy. Results : C. setidens contains pectolinarin and its glycoside, pectolinarigenin as index compounds, and linarin, apigenin, diosmetin, scopoletin, acacetin, cirsimarin, cirsimaritin, setidenosides A and B, silymarin, hispidulin, 92 volatile compounds, and 15 fatty acids. The Pharmacological activities of C. setidens has been reported to inhibit of platelet aggregation and fat accumulation in the liver, inhibit to hepatitis, anti-cancer, antibacterial, skin improvement, hair growth, liver protection, anti-diabetic, anti-inflammatory, sedative. Also, It has been reported the effect of cholesterol-lowering and anti-obesity, neuroprotective effects, increasing human stem cell viability, inhibiting osteoclast formation and osteogenic differentiation. Conclusion : This reviews showed that C. setidens which has been traditionally used for the treatment of inflammation and hypertension, has anticancer and river protective effect, as well as hair loss and diet. In order to maximize the efficacy of C. setidens, research has also begun on the effect of processing processes such as fermentation or fine powdering and combining natural plant resources.

• Journal of Life Science
• /
• v.28 no.12
• /
• pp.1448-1454
• /
• 2018

Insects have been investigated as a novel source of food and biomaterial in several recent studies. However, their osteoblastogenic cell activity has not been sufficiently researched and so, to investigate the potential of this natural material for promoting osteoblastogenesis, we studied the activity of Locusta migratoria ethanol extract (LME) on MG-63 pre-osteoblast cells. The cytotoxicity and proliferation effects of LME on MG-63 cells were measured by MTS assay, and there was no cytotoxicity up to $1,000{\mu}g/ml$. With LME treatment of 500 and $1,000{\mu}g/ml$ for 48 hr, cell proliferation increased to 105% and 116% versus control, respectively. The osteoblastogenic activity of the LME was measured through alkaline phosphatase (ALP) staining at three and five days. As a result, both 500 and $1,000{\mu}g/ml$ LME concentrations were seen to increase ALP activity by more than three times compared with control at three and five days. In addition, the expression level of the osteogenic markers ALP and RUNX2 was markedly increased after LME treatment. These results demonstrate that Locusta migratoria ethanol extract promotes osteoblastogenesis as evidenced by the increased osteogenic markers and suggest that LME may be a potential agent for bone formation and osteoporosis prevention.

• Maxillofacial Plastic and Reconstructive Surgery
• /
• v.27 no.1
• /
• pp.16-23
• /
• 2005

It is commonly acknowledged that bone morphogenic protein (BMP-2) functions as a potential osteogenic inducer in bone formation. Recently, several papers reported that bone marrow-derived stem cell (BMSC) from human is not responsive to BMP-2 in comparison to high capacity of BMP-2 in the osteoinduction of stromal cell derived from bone marrow of rodent animals such as rat or mouse. In this study, we characterized BMSC derived from 11 years old donor for the responsiveness to rhBMP-2, dexamethasone (Dex) and 1,25-dihydroxyvitamin D (vitamin D), in order to analyze their function in the early osteogenesis. The effect of over mentioned agents was evaluated by means of assessing alkaline phosphatase (ALP) activity/staining, RT-PCR analysis and von Kossa staining. In addition, we analyzed the meaning of expressed several osteoblastic markers such as alkaline phosphatase, collagen typeI, osteopontin, bone sialoprotein and osteocalcin with relation to either differentiation or mineralization. Only in the presence of Dex, human BMSC could commit osteoblastic differentiation and matrix mineralization, and either BMP-2 or vitamin D treatment was not able to induce. But BMP-2 or Vitamin D showed potential synergy effect with Dex. ALP and bone sialoprotein were clearly expressed in response of Dex treatment compared to weak expression of osteopontin in early osteogenesis. Therefore, we expect that this study will contribute partly to elucidiating early osteogenesis mechanism in human, but variations among bone marrow donors must be considered through further study.

• Journal of Periodontal and Implant Science
• /
• v.50 no.5
• /
• pp.291-302
• /
• 2020

Purpose: The objective of this study was to investigate whether phelligridin D could reduce glucose-induced oxidative stress, attenuate the resulting inflammatory response, and restore the function of human periodontal ligament cells (HPDLCs). Methods: Primary HPDLCs were isolated from healthy human teeth and cultured. To investigate the effect of phelligridin D on glucose-induced oxidative stress, HPDLCs were treated with phelligridin D, various concentrations of glucose, and glucose oxidase. Glucose-induced oxidative stress, inflammatory molecules, osteoblast differentiation, and mineralization of the HPDLCs were measured by hydrogen peroxide (H₂O₂) generation, cellular viability, alkaline phosphatase (ALP) activity, alizarin red staining, and western blot analyses. Results: Glucose-induced oxidative stress led to increased production of H₂O₂, with negative impacts on cellular viability, ALP activity, and calcium deposition in HPDLCs. Furthermore, HPDLCs under glucose-induced oxidative stress showed induction of inflammatory molecules (intercellular adhesion molecule-1, vascular cell adhesion protein-1, tumor necrosis factor-alpha, interleukin-1-beta) and disturbances of osteogenic differentiation (bone morphogenetic protein-2, and -7, runt-related transcription factor-2), cementogenesis (cementum protein-1), and autophagy-related molecules (autophagy related 5, light chain 3 I/II, beclin-1). Phelligridin D restored all these molecules and maintained the function of HPDLCs even under glucose-induced oxidative stress. Conclusions: This study suggests that phelligridin D reduces the inflammation that results from glucose-induced oxidative stress and restores the function of HPDLCs (e.g., osteoblast differentiation) by upregulating autophagy.

• Journal of dental hygiene science
• /
• v.15 no.4
• /
• pp.488-494
• /
• 2015

A recent report showed that nuclear factor of activated T cell (NFATc) 1 is a member of the NFAT family and is strictly implicated osteoblast differentiation and bone formation. Furthermore, the precise expression and function of NFATc1 in periodontal tissue remains unclear. Therefore, the purpose of this study was to investigate the function of NFATc1 in osteoblastic differentiation, and the underlying mechanism regulating periodontal regeneration in human periodontal ligament cells (hPDLCs). NFATc1 messenger RNA (mRNA) and protein levels were accessed by reverse transcription-polymerase chain reaction (RT-PCR) and western blot assay, respectively. Cell proliferation determined using MTT assay. Differentiation was evaluated by alkaline phosphatase activity and formation of calcium nodule with alizarin red S staining. The mRNA expression of osteoblastic differentiation related genes were examined by RT-PCR. Marked upregulation of NFATc1 mRNA and protein was observed in cells grown in osteogenic medium (OS). NFATc1 transactivation was detected in hPDLCs that had been incubated in OS for 14 days. Treatment with $10{\mu}M$ cyclosporine A (CsA), a known calcineurin inhibitor, reduced the proliferation of hPDLCs, while $5{\mu}M$ CsA had no effect. Inhibition of the calcineurin/NFATc1 pathway by CsA, attenuated OS-induced osteoblastic differentiation in hPDLCs. In summary, this study demonstrates for the first time that NFATc1 plays a key role in osteoblastic differentiation of hPDLCs and activation of NFATc1 could provide a novel mechanism for periodontal bone regeneration.

• Journal of dental hygiene science
• /
• v.19 no.3
• /
• pp.198-204
• /
• 2019

Background: Oxidative stress is a known to be associated with in the pathogenesis of many inflammatory diseases, including periodontitis. Ursolic acid is a pentacyclic triterpenoid with has antimicrobial, antioxidative, and anticancer properties. However, the role of ursolic acid in the regulating of osteogenesis remains undetermined. This study was aimed to elucidate the crucial osteogenic effects of ursolic acid and its ability to inhibit oxidative stress by targeting the immediate early response 3 (IER3)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Methods: Cell proliferation was determined using water-soluble tetrazolium salt assay, cell differentiation was evaluated by alkaline phosphatase (ALP) activity, and formation of calcium nodules was detected using alizarin red S stain. Generation of reactive oxygen species (ROS) was determined using by DCFH-DA fluorescence dye in hydrogen peroxide ($H_2O_2$)-treated MG-63 cells. Expression levels of IER3, Nrf2, and heme oxygenase-1 (HO-1) were analyzed using western blot analysis. Results: Our results showed that ursolic acid up-regulated the proliferation of osteoblasts without any cytotoxic effects, and promoted ALP activity and mineralization. $H_2O_2$-induced ROS generation was found to be significantly inhibited on treatment with ursolic acid. Furthermore, in $H_2O_2$-treated cells, the expression of the early response genes: IER3, Nrf2, and Nrf2-related phase II enzyme (HO-1) was enhanced in the presence of ursolic acid. Conclusion: The key findings of the present study elucidate the protective effects of ursolic acid against oxidative stress conditions in osteoblasts via the IER3/Nrf2 pathway. Thus, ursolic acid may be developed as a preventative and therapeutic agent for mineral homeostasis and inflammatory diseases caused due to oxidative injury.

• Advances in nano research
• /
• v.14 no.6
• /
• pp.507-519
• /
• 2023

Postsurgical infections are caused by implant-related pathogenic microorganisms that lead to graft rejection. Hence, an intrinsically antibacterial material is required to produce a biocompatible biomaterial with osteogenic properties that could address this major issue. Hence, this current research aims to make strontium-doped hydroxyapatite nanorods (SrHANRs) via an ethylene diamine tetraacetic acid (EDTA)-enable microwave mediated method using Anodontia alba seashells for biomedical applications. This investigation also perceives that EDTA acts as a soft template to accomplish Sr-doping and mesoporous structures in pure hydroxyapatite nanorods (HANRs). The X-ray diffraction (XRD) and transmission electron microscopy (TEM) analysis reveals the crystalline and mesoporous structures, and Brunauer-Emmett-Teller (BET) indicates the surface area of all the samples, including pure HANRs and doped HANRs. In addition, the biocidal ability was tested using various implant-related infectious bacteria pathogens, and it was discovered that Sr-doped HANRs have excellent biocidal properties. Furthermore, toxicity evaluation using zebrafish reports the non-toxic nature of the produced HANRs. Incorporating Sr²⁺ ions into the HAp lattice would enhance biocompatibility, biocidal activity, and osteoconductive properties. As a result, the biocompatible HANRs materials synthesized with Sr-dopants may be effective in bone regeneration and antibacterial in-built implant applications.

• Nutrition Research and Practice
• /
• v.18 no.4
• /
• pp.479-497
• /
• 2024

BACKGROUND/OBJECTIVES: Activating brown adipose tissue (BAT) and browning of white adipose tissue (WAT) can protect against obesity and obesity-related metabolic conditions. Cryptotanshinone (CT) regulates lipid metabolism and significantly ameliorates insulin resistance. Adenosine-5'-monophosphate (AMP)-activated protein kinase (AMPK), a receptor for cellular energy metabolism, is believed to regulate brown fat activity in humans. MATERIALS/METHODS: The in vivo study included high-fat-fed obese mice administered orally 200/400 mg/kg/d CT. They were evaluated through weight measurement, the intraperitoneal glucose tolerance test (IPGTT), intraperitoneal insulin tolerance test (IPITT), cold stimulation test, serum lipid (total cholesterol, triglycerides, and low-density lipoprotein) measurement, hematoxylin and eosin staining, and immunohistochemistry. Furthermore, the in vitro study investigated primary adipose mesenchymal stem cells (MSCs) with incubation of CT and AMPK agonists (acadesine)/inhibitor (Compound C). Cells were evaluated using Oil Red O staining, Alizarin red staining, flow cytometry, and immunofluorescence staining to identify and observe the osteogenic versus adipogenic differentiation. Quantitative real-time polymerase chain reaction and the Western blot were used to observe related gene expression. RESULTS: In the diet-induced obesity mouse model mice CT suppressed body weight, food intake, glucose levels in the IPGTT and IPTT, serum lipids, the volume of adipose tissue, and increased thermogenesis, uncoupling protein 1, and the AMPK pathway expression. In the in vitro study, CT prevented the formation of lipid droplets from MSCs while activating brown genes and the AMPK pathway. AMPK activator enhanced CT's effects, while the AMPK inhibitor reversed the effects of CT. CONCLUSION: CT promotes adipose tissue browning to increase body thermogenesis and reduce obesity by activating the AMPK pathway. This study provides an experimental foundation for the use of CT in obesity treatment.

• Maxillofacial Plastic and Reconstructive Surgery
• /
• v.20 no.2
• /
• pp.139-147
• /
• 1998

This study has been performed to evaluate the relationship between the remained mineral components in a decalcified bone matrix and an ectopic bone formation efficiency. The freezed rat diaphyseal cortical bones measuring 0.5cm in length were demineralized in heated 0.6N HCl at $60^{\circ}C$ for 5, 10, 15, 20, 25, 30, 35, 40 minutes, respectively, using a controlled heat ultrasonic cleaner. Each 1cc of decalcifying solution taken during decalcification procedure was used to calculate calcium content using calcium dignostics kit under 600nm of spectrophotomer. After decalcification, each specimen was also weighed. Then each prepared specimen was implanted into the dorsal pouch of 24 Sprague-Dawley rats divided into 8 groups by time course. The implants were harvested at 1, 2, and 3 weeks and prepared for routine H-E stain specimens to evaluate osteogenic activity. The results are as follows: 1. There was statistical significant difference in change of calcium concentration up to demineralization of 30 minutes and each allogenic bones decalcifed up to 20 minutes revealed 99.65% of decalcification in average. 2. There was statistical significant difference in change of weight in demineralized allogenic bone up to 20 minutes treatment but, no significant change was noted after that time. 3. The histologic analysis revealed active ectopic bone formation in the implanted allografts demineralized for 20, 25, 30 minutes, respectively. However, the other groups of allografts showed relatively poor osteoinductive activity. These findings suggest that complete decalcification with a minimized degeneration of collagen matrix is necessary to induce maximal osteogenesis by decalcified bone allograft.

• Journal of Periodontal and Implant Science
• /
• v.39 no.sup2
• /
• pp.279-286
• /
• 2009

Purpose: Gene therapy (ex vivo) has recently been used as a means of delivering bone morphogenetic proteins (BMPs) to sites of tissue regeneration. In the present study, we investigated the effect of co-transduction of adenoviruses expressing BMP-2 and BMP-7 on osteogenesisof C2C12 cells in vitro. Methods: A replication-defective human adenovirus 5 (Ad5) containing a cDNA for BMPs in the E1 region of the virus (Ad5BMP-2 and Ad5BMP-7) was constructed by in vivo homologous recombination. Functional activity of Ad5BMP-2 and Ad5BMP-7 were evaluated in mouse stromal cells (W20-17cells). C2C12 cells are transduced with various MOI (multiplicity of infection) of Ad5BMP-2 and Ad5BMP-7 to assess most effective and stable titer. Based on this result, C2C12 cells were transduced with Ad5BMP-2 and Ad5BMP-7 alone or by combination. BMPs expression, alkaline phosphatase (ALPase) activity, cell proliferation, and mineralization were assessed. Results: Ad5BMP-2 and Ad5BMP-7 are successfully transduced to W20-17 cells, and secreted BMPs stimulated cell differentiation. Also, C2C12 cells transduced with Ad5BMPs showed expression of BMPs and increased ALPaseactivity. In all groups, cell proliferation was observed over times. At 7days, cells co-transduced with Ad5BMP-2 and Ad5BMP-7 showed lower proliferation than the others. C2C12 cells co-transduced with Ad5BMP-2 and Ad5BMP-7 had greater ALPaseactivity than that would be predicted if effect of individual Ad5BMPs were additive. Little mineralized nodule formation was detected in cells transduced with individual Ad5BMPs. In contrast, Ad5BMP-2 and Ad5BMP-7 combination stimulated mineralization after culturing for 10 days in mineralizing medium. Conclusions: Present study demonstrated that adenoviruses expressing BMPs gene successfully produced BMPs protein and these BMPs stimulated cells to be differentiated into osteoblastic cells. In addition, the osteogenic activity of Ad5BMPs can be synergistically increased by co-transduction of cells with Ad5BMP-2 and Ad5BMP-7.