84年鼠女哪年财运最旺,857comvvv色九欧美激情|85PO_87国产精品欲av国产av资源

[1]蘇珮茹,羅香雅,余麗娜,等.紫菀酮對體外破骨細(xì)胞分化和活性的影響及作用機(jī)制研究[J].中醫(yī)正骨,2023,35(06):24-35.
　SU Peiru,LUO Xiangya,YU Lina,et al.Effects of shionone on differentiation and activity of osteoclasts in vitro and its mechanism of action[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2023,35(06):24-35.
點(diǎn)擊復(fù)制

紫菀酮對體外破骨細(xì)胞分化和活性的影響及作用機(jī)制研究()
分享到：

《中醫(yī)正骨》[ISSN:1001-6015/CN:41-1162/R]

卷:
第35卷
期數(shù):
2023年06期
頁碼:
24-35
欄目:
基礎(chǔ)研究
出版日期:
2023-06-20

文章信息/Info

Title:
Effects of shionone on differentiation and activity of osteoclasts in vitro and its mechanism of action
作者:
蘇珮茹1; 羅香雅1; 余麗娜2; 曾春平1; 周琳1
(1.廣州醫(yī)科大學(xué)附屬第五醫(yī)院,廣東 廣州 510700; 2.華北理工大學(xué)公共衛(wèi)生學(xué)院,河北 唐山 063210)
Author(s):
SU Peiru1; LUO Xiangya1; YU Lina2; ZENG Chunping1; ZHOU Lin1
1.The Fifth Affiliated Hospital of Guangzhou Medical University,Guangzhou 510700,Guangdong,China 2.School of Public Health,North China University of Science and Technology,Tangshan 063210,Hebei,China
關(guān)鍵詞:
骨質(zhì)疏松;  破骨細(xì)胞;  細(xì)胞分化;  紫菀酮;  體外研究技術(shù);  信號傳導(dǎo);  NF-κB;  組織蛋白酶K;  腺苷三磷酸酶;  抗酒石酸酸性磷酸酶;  NFATC轉(zhuǎn)錄因子
Keywords:
osteoporosis;  osteoclasts;  cell differentiation;  shionone;  in vitro techniques;  signal transduction;  NF-kappa B;  Cathepsin K;  adenosine triphosphatases;  tartrate-resistant acid phosphatase;  NFATC transcription factors
摘要:
目的:探討紫菀酮對體外破骨細(xì)胞分化和活性的影響及作用機(jī)制。方法:①分析紫菀酮對核因子-κB受體活化因子配體(receptor activator of nuclear factor-κB ligand,RANKL)誘導(dǎo)Raw 264.7細(xì)胞向破骨細(xì)胞分化的影響。將Raw 264.7細(xì)胞分為空白對照組、陽性對照組、紫菀酮1 μmol·L-1干預(yù)組、紫菀酮2.5 μmol·L-1干預(yù)組、紫菀酮5 μmol·L-1干預(yù)組和紫菀酮10 μmol·L-1干預(yù)組,空白對照組加入完全培養(yǎng)基,陽性對照組加入含25 ng·mL-1RANKL的完全培養(yǎng)基,其余各組分別加入含有相應(yīng)濃度紫菀酮及25 ng·mL-1RANKL的完全培養(yǎng)基,培養(yǎng)5 d后進(jìn)行抗酒石酸酸性磷酸酶(tartrate-resistant acid phosphatase,TRAP)染色,統(tǒng)計(jì)各組破骨細(xì)胞數(shù); ②分析紫菀酮對Raw 264.7細(xì)胞活力的影響。將Raw 264.7細(xì)胞分為空白對照組、紫菀酮1 μmol·L-1干預(yù)組、紫菀酮2.5 μmol·L-1干預(yù)組、紫菀酮5 μmol·L-1干預(yù)組和紫菀酮10 μmol·L-1干預(yù)組,空白對照組加入完全培養(yǎng)基,其余各組分別加入含有相應(yīng)濃度紫菀酮的完全培養(yǎng)基,分別培養(yǎng)48 h、120 h后測定各組細(xì)胞活力; ③分析紫菀酮對破骨細(xì)胞纖維狀肌動蛋白環(huán)形成的影響。將Raw 264.7細(xì)胞分為空白對照組、陽性對照組、紫菀酮5 μmol·L-1干預(yù)組和紫菀酮10 μmol·L-1干預(yù)組,空白對照組加入完全培養(yǎng)基,陽性對照組加入含25 ng·mL-1RANKL的完全培養(yǎng)基,紫菀酮5 μmol·L-1干預(yù)組和紫菀酮10 μmol·L-1干預(yù)組分別加入含有相應(yīng)濃度紫菀酮及25 ng·mL-1RANKL的完全培養(yǎng)基,培養(yǎng)5 d后采用鬼筆環(huán)肽和4',6-二脒基-2-苯基吲哚染色,觀察各組破骨細(xì)胞纖維狀肌動蛋白環(huán)形成情況。④分析紫菀酮對核因子-κB(nuclear factor-κB,NF-κB)轉(zhuǎn)錄活性的影響。將穩(wěn)定轉(zhuǎn)染pGL4.32[luc2P/NF-κB-RE/Hygro]載體的RAW 264.7細(xì)胞分為空白對照組、陽性對照組和紫菀酮 10 μmol·L-1干預(yù)組,空白對照組及陽性對照組加入完全培養(yǎng)基,紫菀酮10 μmol·L-1干預(yù)組加入終濃度為10 μmol·L-1紫菀酮的完全培養(yǎng)基; 培養(yǎng)2 h后,陽性對照組及紫菀酮10 μmol·L-1干預(yù)組分別加入RANKL溶液,使培養(yǎng)基中RANKL的終濃度為25 ng·mL-1; 繼續(xù)培養(yǎng)6 h后,檢測各組細(xì)胞熒光素酶的熒光強(qiáng)度。⑤分析紫菀酮對核因子-κB抑制蛋白激酶α亞基(inhibitor of nuclear factor kappa-B kinase subunit α,IκBα)蛋白表達(dá)的影響。將Raw 264.7細(xì)胞分為陽性對照組和紫菀酮10 μmol·L-1干預(yù)組,每組6孔,分別編號1～6。待細(xì)胞貼壁后,陽性對照組加入完全培養(yǎng)基,紫菀酮10 μmol·L-1干預(yù)組加入終濃度為10 μmol·L-1紫菀酮的完全培養(yǎng)基,繼續(xù)培養(yǎng)2 h后,在2組的1號孔加入RANKL溶液使RANKL終濃度為25 ng·mL-1,在1號孔加入RANKL溶液后30 min、40 min、50 min、55 min,分別在2號、3號、4號、5號孔加入RANKL溶液至RANKL終濃度為25 ng·mL-1。在1號孔加入RANKL后60 min,收集各孔細(xì)胞,采用蛋白印跡法檢測IκBα蛋白的表達(dá)量。⑥分析紫菀酮對破骨細(xì)胞特異性基因轉(zhuǎn)錄的影響。將Raw 264.7細(xì)胞分為陽性對照組、紫菀酮5 μmol·L-1干預(yù)組和紫菀酮10 μmol·L-1干預(yù)組。陽性對照組加入含 25 ng·mL-1RANKL的完全培養(yǎng)基,紫菀酮5 μmol·L-1干預(yù)組和紫菀酮10 μmol·L-1干預(yù)組分別加入含有相應(yīng)濃度紫菀酮和25 ng·mL-1RANKL的完全培養(yǎng)基,培養(yǎng)5 d后,收集各組細(xì)胞,采用實(shí)時(shí)定量PCR檢測組織蛋白酶K、空泡型ATP酶d2亞基(vacuolar ATPase subsnit D2,V-ATPase d2)、TRAP的mRNA表達(dá)量。⑦分析紫菀酮對活化T-細(xì)胞核因子c1(nuclear factor of activated T cells c1,NFATc1)蛋白表達(dá)的影響。將Raw 264.7細(xì)胞分為陽性對照組和紫菀酮10 μmol·L-1干預(yù)組,每組4孔,分別編號1～4。待細(xì)胞貼壁后,陽性對照組加入完全培養(yǎng)基,紫菀酮10 μmol·L-1干預(yù)組加入終濃度為10 μmol·L-1紫菀酮的完全培養(yǎng)基。繼續(xù)培養(yǎng)2 h后,在2組的1號孔加入RANKL溶液使RANKL終濃度為25 ng·mL-1,在1號孔加入RANKL溶液后2 d、4 d,分別在2號、3號孔加入RANKL溶液使RANKL終濃度為25 ng·mL-1。在1號孔加入RNAKL后5 d,收集各孔細(xì)胞。采用蛋白印跡法檢測NFATc1蛋白的表達(dá)量。結(jié)果:①紫菀酮對RANKL誘導(dǎo)Raw 264.7細(xì)胞向破骨細(xì)胞分化影響的分析結(jié)果。空白對照組之外的5組破骨細(xì)胞數(shù)比較,差異有統(tǒng)計(jì)學(xué)意義[(187.667±14.503)個,(180.000±14.422)個,(174.333±11.060)個,(152.667±5.033)個,(130.667±11.015)個,F=11.767,P=0.001]。紫菀酮10 μmol·L-1干預(yù)組、紫菀酮5 μmol·L-1干預(yù)組破骨細(xì)胞數(shù)均少于陽性對照組、紫菀酮1 μmol·L-1干預(yù)組和紫菀酮2.5 μmol·L-1干預(yù)組(P=0.004,P=0.000; P=0.017,P=0.000; P=0.047,P=0.001); 紫菀酮10 μmol·L-1干預(yù)組破骨細(xì)胞數(shù)少于紫菀酮5 μmol·L-1干預(yù)組(P=0.044)。②紫菀酮對Raw 264.7細(xì)胞活力影響的分析結(jié)果。紫菀酮干預(yù)48 h、120 h時(shí),5組Raw 264.7細(xì)胞活力比較,組間差異均無統(tǒng)計(jì)學(xué)意義(48 h:0.960±0.101,0.938±0.051,0.916±0.072,0.915±0.079,1.009±0.105,F=0.647,P=0.641; 120 h:1.347±0.161,1.388±0.047,1.423±0.473,1.398±0.067,1.357±0.034,F=0.400,P=0.805)。③紫菀酮對破骨細(xì)胞纖維狀肌動蛋白環(huán)形成影響的分析結(jié)果。與空白對照組比較,陽性對照組、紫菀酮5 μmol·L-1干預(yù)組和紫菀酮10 μmol·L-1干預(yù)組均可見破骨細(xì)胞和纖維狀肌動蛋白環(huán); 與陽性對照組比較,紫菀酮5 μmol·L-1干預(yù)組和紫菀酮10 μmol·L-1干預(yù)組破骨細(xì)胞纖維狀肌動蛋白環(huán)形成均受到抑制,且其受到抑制的程度隨紫菀酮干預(yù)濃度增加而增強(qiáng)。④紫菀酮對破骨細(xì)胞NF-κB轉(zhuǎn)錄活性影響的分析結(jié)果。3組熒光素酶相對熒光強(qiáng)度比較,組間差異有統(tǒng)計(jì)學(xué)意義(0.058±0.003,1.000±0.044,0.753±0.040,F=613.132,P=0.000)。陽性對照組和紫菀酮10 μmol·L-1干預(yù)組的熒光素酶相對熒光強(qiáng)度高于空白對照組(P=0.000,P=0.000),紫菀酮10 μmol·L-1干預(yù)組的熒光素酶熒光強(qiáng)度低于陽性對照組(P=0.000)。⑤紫菀酮對IκBα蛋白表達(dá)影響的分析結(jié)果。2組破骨細(xì)胞IκBα蛋白相對表達(dá)量隨誘導(dǎo)時(shí)間延長均呈先下降后上升趨勢,但2組的趨勢不完全一致(1.000±0.000,0.414±0.171,0.285±0.104,0.132±0.021,0.157±0.038,0.802±0.066,F=49.839,P=0.000; 0.980±0.130,0.632±0.102,0.347±0.037,0.302±0.070,0.546±0.142,1.502±0.345,F=21.435,P=0.000); 誘導(dǎo)20 min、30 min、60 min,紫菀酮10 μmol·L-1干預(yù)組破骨細(xì)胞IκBα蛋白相對表達(dá)量高于陽性對照組(t=-4.018,P=0.016; t=-4.586,P=0.010; t=-3.444,P=0.026)。⑥紫菀酮對破骨細(xì)胞特異性基因轉(zhuǎn)錄影響的分析結(jié)果。3組破骨細(xì)胞V-ATPase-d2、組織蛋白酶K、TRAP的mRNA表達(dá)量比較,組間差異均有統(tǒng)計(jì)學(xué)意義(1.000±0.089,0.879±0.100,0.530±0.054,F=25.553,P=0.001; 1.000±0.030,0.725±0.153,0.719±0.111,F=6.293,P=0.034; 1.000±0.326,0.834±0.030,0.656±0.327,F=88.003,P=0.000)。紫菀酮5 μmol·L-1干預(yù)組破骨細(xì)胞組織蛋白酶K、TRAP的mRNA表達(dá)量均低于陽性對照組(P=0.023,P=0.001); 紫菀酮10 μmol·L-1干預(yù)組破骨細(xì)胞V-ATPase-d2、TRAP的mRNA表達(dá)量均低于紫菀酮5 μmol·L-1干預(yù)組和陽性對照組(P=0.000,P=0.002; P=0.000,P=0.000); 紫菀酮10 μmol·L-1干預(yù)組破骨細(xì)胞組織蛋白酶K的mRNA表達(dá)量低于陽性對照組(P=0.021)。⑦紫菀酮對NFATc1蛋白表達(dá)影響的分析結(jié)果。2組破骨細(xì)胞NFATc1蛋白相對表達(dá)量隨誘導(dǎo)時(shí)間延長均呈上升趨勢,但2組的上升趨勢不完全一致(1.000±0.000,1.175±0.007,4.700±0.742,19.430±1.763,F=250.352,P=0.000; 1.042±0.035,1.334±0.290,3.531±0.583,15.690±0.823,F=525.669,P=0.000); 誘導(dǎo)后5 d,紫菀酮10 μmol·L-1干預(yù)組破骨細(xì)胞NFATc1蛋白相對表達(dá)量低于陽性對照組(t=3.329,P=0.029)。結(jié)論:紫菀酮能夠抑制體外破骨細(xì)胞的分化和活性,其作用機(jī)制與抑制NF-κB和NFATc1信號通路有關(guān)。
Abstract:
Objective:To explore the effects of shionone on differentiation and activity of osteoclasts in vitro and its mechanism of action.Methods:①To analyze the effects of shionone on the differentiation of Raw 264.7 cells into osteoclasts induced by receptor activator of nuclear factor-κB ligand(RANKL).The Raw 264.7 cells were divided into blank control group,positive control group,1 μmol/L shionone intervention group,2.5 μmol/L shionone intervention group,5 μmol/L shionone intervention group and 10 μmol/L shionone intervention group.The Raw 264.7 cells in blank control group were cultured in complete culture medium,the ones in positive control group were cultured in complete culture medium supplemented with 25 ng/mL RANKL,and the ones in the rest groups were cultured in complete culture medium supplemented with 25 ng/mL RANKL and shionone at concentration of 1,2.5,5 and 10 μmol/L respectively.After 5-day culture,tartrate-resistant acid phosphatase(TRAP)staining was performed,and the number of osteoclasts in each group was counted.②To analyze the effects of shionone on the viability of Raw 264.7 cells.The Raw 264.7 cells were divided into blank control group,1 μmol/L shionone intervention group,2.5 μmol/L shionone intervention group,5 μmol/L shionone intervention group and 10 μmol/L shionone intervention group.The Raw 264.7 cells in blank control group were cultured in complete culture medium,and the ones in the other groups were cultured in complete culture medium supplemented with shionone at concentration of 1,2.5,5 and 10 μmol/L respectively.After 48- and 120-hour culture,the viability of Raw 264.7 cells were detected in each group.③To analyze the effects of shionone on the formation of fibrous actin rings(F-actin rings)in osteoclasts.The Raw 264.7 cells were divided into blank control group,positive control group,5 μmol/L shionone intervention group and 10 μmol/L shionone intervention group.The Raw 264.7 cells in blank control group were cultured in complete culture medium,the ones in positive control group were cultured in complete culture medium supplemented with 25 ng/mL RANKL,and the ones in the remained 2 groups were cultured in complete culture medium supplemented with 25 ng/mL RANKL and shionone at concentration of 5 and 10 μmol/L respectively.After 5-day culture,the staining was performed with phalloidin and 4',6-diamidino-2-phenylindole(DAPI)to observe the formation of F-actin rings in osteoclasts in each group.④To analyze the effects of shionone on the transcriptional activity of nuclear factor-κB(NF-κB).The RAW 264.7 cells stably transfected with pGL4.32[luc2P/NF-κB-RE/Hygro] vector were divided into blank control group,positive control group and 10 μmol/L shionone intervention group.The transfected cells in blank control group and positive control group were cultured in complete culture medium,and the ones in 10 μmol/L shionone intervention group were cultured in complete culture medium supplemented with shionone at final concentration of 10 μmol/L.After 2-hour culture,the cells in positive control group and 10 μmol/L shionone intervention group were added with RANKL solution respectively till its final concentration was 25 ng/mL in the medium.After an additional 6-hour culture,the fluorescence intensity of luciferase in each group was detected.⑤To analyze the effects of shionone on the protein expression of inhibitor of nuclear factor kappa-B kinase subunit α(IκBα).The Raw 264.7 cells were divided into positive control group and 10 μmol/L shionone intervention group,with 6 wells in each group numbered from 1 to 6 respectively.After cell adhesion,the cells in positive control group were cultured in complete culture medium,and the ones in 10 μmol/L shionone intervention group were cultured in complete culture medium supplemented with shionone at final concentration of 10μmol/L.After an additional 2-hour culture,the No.1 wells in the 2 groups were added with RANKL solution respectively till its final concentration was 25 ng/mL in the medium.At 30,40,50,and 55 minutes after adding RANKL solution to the No.1 wells,the No.2,3,4 and 5 wells in the 2 groups were added with RANKL solution respectively till its final concentration was 25 ng/mL in the medium.At 60 minutes after adding RANKL to the No.1 wells,the cells were collected from each well,and the protein expression level of IκBα was detected by using Western blot.⑥To analyze the effects of shionone on the transcription of osteoclast-specific genes.The Raw 264.7 cells were divided into positive control group,5 μmol/L shionone intervention group and 10 μmol/L shionone intervention group.The cells in positive control group were cultured in complete culture medium supplemented with 25 ng/mL RANKL,and the ones in the other two groups were cultured in complete culture medium supplemented with 25 ng/mL RANKL and shionone at concentration of 5 and 10 μmol/L respectively.After 5-day culture,the cells were collected from each group,and the mRNA expression levels of cathepsin K,vacuolar ATPase subunit D2(V-ATPase d2)and TRAP were detected by using real-time quantitative PCR(RT-qPCR).⑦To analyze the effects of shionone on the protein expression of nuclear factor of activated T cells c1(NFATc1).The Raw 264.7 cells were divided into positive control group and 10 μmol/L shionone intervention group,with 4 wells in each group numbered from 1 to 4 respectively.After cell adhesion,the cells in positive control group were cultured in complete culture medium,and the ones in 10 μmol/L shionone intervention group were cultured in complete culture medium supplemented with shionone at final concentration of 10 μmol/L.After an additional 2-hour culture,the No.1 wells in the 2 groups were added with RANKL solution respectively till its final concentration was 25 ng/mL in the medium.At 2 and 4 days after adding RANKL solution to the No.1 wells,the No.2 and 3 wells in the 2 groups were added with RANKL solution respectively till its final concentration was 25 ng/mL in the medium.At 5 days after adding RANKL solution to the No.1 wells,the cells were collected from each well,and the protein expression level of NFATc1 was detected by using Western blot.Results:①The results of analysis on the effects of shionone on RANKL-induced differentiation of Raw 264.7 cells into osteoclasts.There was statistical difference in the number of osteoclasts among the 5 groups except for the blank control group(187.667±14.503,180.000±14.422,174.333±11.060,152.667±5.033,130.667±11.015,F=11.767,P=0.001).The number of osteoclasts was less in 10 μmol/L shionone intervention group and 5 μmol/L shionone intervention group compared to positive control group,1 μmol/L shionone intervention group and 2.5 μmol/L shionone intervention group(P=0.004,P=0.000; P=0.017,P=0.000; P=0.047,P=0.001),and it was less in 10 μmol/L shionone intervention group compared to 5 μmol/L shionone intervention group(P=0.044).②The results of analysis on the effects of shionone on the viability of Raw 264.7 cells.There was no statistical difference in the viability of Raw 264.7 cells among the 5 groups after 48- and 120-hour intervention(48-hour:0.960±0.101,0.938±0.051,0.916±0.072,0.915±0.079,1.009±0.105,F=0.647,P=0.641; 120-hour:1.347±0.161,1.388±0.047,1.423±0.473,1.398±0.067,1.357±0.034,F=0.400,P=0.805).③The results of analysis on the effects of shionone on the formation of F-actin rings in osteoclasts.Compared with the blank control group,the osteoclasts and F-actin rings were observed in positive control group,5 μmol/L shionone intervention group and 10 μmol/L shionone intervention group.Compared with the positive control group,the formation of F-actin rings in osteoclasts was inhibited in 5 μmol/L shionone intervention group and 10 μmol/L shionone intervention group,and the degree of inhibition enhanced with the increasement of intervention concentration of shionone.④The results of analysis on the effects of shionone on the NF-κB transcriptional activity in osteoclasts.There was statistical difference in the relative fluorescence intensity of luciferase among the 3 groups(0.058±0.003,1.000±0.044,0.753±0.040,F=613.132,P=0.000).The relative fluorescence intensity of luciferase was higher in positive control group and 10 μmol/L shionone intervention group compared to blank control group(P=0.000,P=0.000),and it was higher in positive control group compared to 10 μmol/L shionone intervention group(P=0.000).⑤The results of analysis on the effects of shionone on the expression of IκBα protein.The relative expression level of IκBα protein in osteoclasts displayed a trend of going downward firstly and upward subsequently with the induction-time in the 2 groups,while the 2 groups were inconsistent with each other in the variation tendency(1.000±0.000,0.414±0.171,0.285±0.104,0.132±0.021,0.157±0.038,0.802±0.066,F=49.839,P=0.000; 0.980±0.130,0.632±0.102,0.347±0.037,0.302±0.070,0.546±0.142,1.502±0.345,F=21.435,P=0.000).The relative expression level of IκBα protein in osteoclasts was higher in 10 μmol/L shionone intervention group compared to positive control group when the cells were induced for 20,30 and 60 minutes respectively(t=-4.018,P=0.016; t=-4.586,P=0.010; t=-3.444,P=0.026).⑥The results of analysis on the effects of shionone on the transcription of osteoclast-specific genes.There was statistical difference in the mRNA expression levels of V-ATPase-d2,cathepsin K and TRAP in osteoclasts among the 3 groups(1.000±0.089,0.879±0.100,0.530±0.054,F=25.553,P=0.001; 1.000±0.030,0.725±0.153,0.719±0.111,F=6.293,P=0.034; 1.000±0.326,0.834±0.030,0.656±0.327,F=88.003,P=0.000).The mRNA expression levels of cathepsin K and TRAP in osteoclasts were lower in 5 μmol/L shionone intervention group compared to positive control group(P=0.023,P=0.001).The mRNA expression levels of V-ATPase-d2 and TRAP in osteoclasts were lower in 10 μmol/L shionone intervention group compared to 5 μmol/L shionone intervention group and positive control group(P=0.000,P=0.002; P=0.000,P=0.000).The mRNA expression level of cathepsin K in osteoclasts was lower in 10 μmol/L shionone intervention group compared to positive control group(P=0.021).⑦The results of analysis on the effects of shionone on the expression of NFATc1 protein.The relative expression level of NFATc1 protein in osteoclasts displayed an upward trend with the induction-time in the 2 groups,while the 2 groups were inconsistent with each other in the variation tendency(1.000±0.000,1.175±0.007,4.700±0.742,19.430±1.763,F=250.352,P=0.000; 1.042±0.035,1.334±0.290,3.531±0.583,15.690±0.823,F=525.669,P=0.000).After 5-day induction,the relative expression level of NFATc1 protein in osteoclasts was lower in 10 μmol/L shionone intervention group compared to positive control group(t=3.329,P=0.029).Conclusion:Shionone can inhibit the differentiation and activity of osteoclasts in vitro,and its mechanism may be that it can inhibit NF-κB and NFATc1 signaling pathways.

參考文獻(xiàn)/References:

[1] 蔡俊民,周后德.免疫性骨質(zhì)疏松及其研究進(jìn)展[J].中華內(nèi)分泌代謝雜志,2022,38(7):558-566.
[2] WANG L,YU W,YIN X,et al.Prevalence of osteoporosis and fracture in China:the China osteoporosis prevalence study[J].JAMA Netw Open,2021,4(8):e2121106.
[3] 陳鏡,馮正平.骨質(zhì)疏松癥治療藥物研究進(jìn)展[J].中國骨質(zhì)疏松雜志,2021,27(5):776-780.
[4] 祝曉雨,張偉光,趙志剛.骨質(zhì)疏松癥國內(nèi)外藥物治療的研究現(xiàn)狀[J].中國臨床藥理學(xué)雜志,2020,36(5):588-592.
[5] KHORSAND I,KASHEF R,GHAZANFARPOUR M,et al.The beneficial and adverse effects of Raloxifene in menopausal women:a mini review[J].J Menopausal Med,2018,24(3):183-187.
[6] REID I R,BILLINGTON E O.Drug therapy for osteoporosis in older adults[J].Lancet,2022,399(10329):1080-1092.
[7] HONG G,CHEN Z,HAN X,et al.A novel RANKL-targeted flavonoid glycoside prevents osteoporosis through inhibiting NFATc1 and reactive oxygen species[J]. Clin Transl Med,2021,11(5):e392.
[8] MARTINIAKOVA M,BABIKOVA M,OMELKA R.Pharmacological agents and natural compounds:available treatments for osteoporosis[J].J Physiol Pharmacol,2020,71(3):307-320.
[9] 韓楊楊,高凡,秦飄然,等.紫菀的研究進(jìn)展及質(zhì)量標(biāo)志物預(yù)測分析[J].中國現(xiàn)代中藥,2023,25(3):655-664.
[10] XU N,HU J,HAN K,et al.Shionone suppresses the growth,migration and invasion of human breast cancer cells via induction of apoptosis and inhibition of MEK/ERK and STAT3 signalling pathways[J].J BUON,2020,25(4):1821-1826.
[11] 鮮恩英,邊巴卓瑪,格央,等.紫菀酮抑制HeLa細(xì)胞遷移侵襲的作用及機(jī)制[J].高原科學(xué)研究,2021,5(2):57-63.
[12] ZHANG B,XUE Y,ZHAO J,et al.Shionone attenuates sepsis-induced acute kidney injury by regulating macrophage polarization via the ECM1/STAT5 pathway[J].Front Med(Lausanne),2022,8:796743.
[13] WANG X,YIN H,FAN L,et al.Shionone alleviates NLRP3 inflammasome mediated pyroptosis in interstitial cystitis injury[J].Int Immunopharmacol,2021,90:107132.
[14] 王芳,任剛,潘玲玲,等.紫菀酮基于NF-κB信號通路的體外抗炎機(jī)制研究[J].中華中醫(yī)藥雜志,2016,31(4):1430-1433.
[15] YAO Z,GETTING S J,LOCKE I C.Regulation of TNF-induced osteoclast differentiation[J].Cells,2021,11(1):132.
[16] YUAN F L,WU Q Y,MIAO Z N,et al.Osteoclast-derived extracellular vesicles:novel regulators of osteoclastogenesis and osteoclast-osteoblasts communication in bone remodeling[J].Front Physiol,2018,9:628.
[17] YAHARA Y,NGUYEN T,ISHIKAWA K,et al.The origins and roles of osteoclasts in bone development,homeostasis and repair[J].Development,2022,149(8):dev199908.
[18] RABJOHNS E M,HURST K,GHOSH A,et al.Paget's di-sease of bone:osteoimmunology and osteoclast pathology[J].Curr Allergy Asthma Rep,2021,21(4):23.
[19] MCDONALD M M,KHOO W H,NG P Y,et al.Osteoclasts recycle via osteomorphs during RANKL-stimulated bone resorption[J].Cell,2021,184(5):1330-1347.
[20] KIM J M,LIN C,STAVRE Z,et al.Osteoblast-osteoclast communication and bone homeostasis[J].Cells,2020,9(9):2073.
[21] YASUDA H.Discovery of the RANKL/RANK/OPG sys-tem[J].J Bone Miner Metab,2021,39(1):2-11.
[22] TAKAYANAGI H.RANKL as the master regulator of osteoclast differentiation[J].J Bone Miner Metab,2021,39(1):13-18.
[23] 艾奎,李楨.紫菀酮改善OVA誘導(dǎo)哮喘SD幼鼠的免疫反應(yīng)及TLRs的表達(dá)[J].中國比較醫(yī)學(xué)雜志,2022,32(9):76-81.
[24] HE J,CHEN K,DENG T,et al.Inhibitory effects of rhaponticin on osteoclast formation and resorption by targeting RANKL-induced NFATc1 and ROS activity[J].Front Pharmacol,2021,12:645140.
[25] TEITELBAUM S L.Bone resorption by osteoclasts[J].Science,2000,289(5484):1504-1508.
[26] LIU Y,WANG C,WANG G,et al.Loureirin B suppresses RANKL-induced osteoclastogenesis and ovariectomized osteoporosis via attenuating NFATc1 and ROS activities[J].Theranostics,2019,9(16):4648-4662.
[27] ONO T,NAKASHIMA T.Recent advances in osteoclast biology[J].Histochem Cell Biol,2018,149(4):325-341.
[28] WINSLOW M M,PAN M,STARBUCK M,et al.Calcineurin/NFAT signaling in osteoblasts regulates bone mass[J].Dev Cell,2006,10(6):771-782.
[29] YANG M,XIE J,LEI X,et al.Tubeimoside I suppresses diabetes-induced bone loss in rats,osteoclast formation,and RANKL-induced nuclear factor-κB pathway[J].Int Immunopharmacol,2020,80:106202.

相似文獻(xiàn)/References:

[1]李林軍.應(yīng)用膨脹式椎弓根螺釘內(nèi)固定治療合并骨質(zhì)疏松的 胸腰椎退行性疾病[J].中醫(yī)正骨,2015,27(08):49.
[2]韓艷,溫利平,劉娜,等.補(bǔ)腎活血方對去卵巢大鼠骨代謝及骨密度的影響[J].中醫(yī)正骨,2015,27(12):7.
　HAN Yan,WEN Liping,LIU Na,et al.Effect of Bushen Huoxue Fang(補(bǔ)腎活血方)on bone metabolism and bone mineral density in the ovariectomized rats[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2015,27(06):7.
[3]李學(xué)朋,朱立國.骨疏康膠囊對去卵巢大鼠骨小梁的影響[J].中醫(yī)正骨,2015,27(12):12.
　LI Xuepeng,ZHU Liguo.Effect of Gushukang Jiaonang(骨疏康膠囊)on bone trabecula in the ovariectomized rats[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2015,27(06):12.
[4]陳冠軍,陳揚(yáng),莊汝杰.可灌注骨水泥椎弓根螺釘系統(tǒng) 在老年腰椎疾患手術(shù)中的應(yīng)用[J].中醫(yī)正骨,2015,27(02):40.
[5]王丹輝,賁越,韓梅.林蛙油治療絕經(jīng)后骨質(zhì)疏松癥的臨床研究[J].中醫(yī)正骨,2014,26(01):27.
　Wang Danhui*,Ben Yue,Han Mei..Clinical study of Rana temporaria oil in the treatment of postmenopausal osteoporosis[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2014,26(06):27.
[6]黃建華,黃建武,李慧輝,等.加味左歸丸對絕經(jīng)后骨質(zhì)疏松癥肝腎不足證 患者骨密度的影響[J].中醫(yī)正骨,2013,25(11):19.
　Huang Jianhua*,Huang Jianwu,Li Huihui,et al.Effect of JIAWEI ZUOGUI pill on bone mineral density in postmenopausal osteoporosis patients with deficiency of liver and kidney[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2013,25(06):19.
[7]項(xiàng)旻,楊虹,林愛菊,等.絕經(jīng)后2型糖尿病患者骨質(zhì)疏松與血微量元素的關(guān)系研究[J].中醫(yī)正骨,2013,25(12):20.
　Xiang Min*,Yang Hong,Lin Aiju,et al.Clinical study on the relationship between osteoporosis and serum trace elements levels in postmenopausal women with type 2 diabetes[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2013,25(06):20.
[8]史曉林,李春雯,張志強(qiáng).弱陽離子磁珠分離技術(shù)和基質(zhì)輔助激光解吸電離飛行時(shí)間質(zhì)譜技術(shù)在原發(fā)性Ⅰ型骨質(zhì)疏松癥血清標(biāo)志蛋白篩選中的應(yīng)用[J].中醫(yī)正骨,2014,26(03):5.
　Shi Xiaolin*,Li Chunwen,Zhang Zhiqiang..Application of magnetic beads based weak cation exchange separation technology and matrix-assisted laser desorption-ionization time of flight mass spectrometry technology in screening serum protein markers of primary type-Ⅰ osteoporosis[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2014,26(06):5.
[9]李明,徐明雄,馮左基,等.自擬壯骨方治療絕經(jīng)后骨質(zhì)疏松癥的療效及作用機(jī)制研究[J].中醫(yī)正骨,2014,26(09):21.
　Li Ming*,Xu Mingxiong,Feng Zuoji,et al.Study on the curative effect and mechanism of action of self-made ZHUANGGU decoction in treatment of postmenopausal osteoporosis[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2014,26(06):21.
[10]陳俊杰,李晴晴,夏瑢.脂代謝及血清內(nèi)脂素水平與絕經(jīng)后骨質(zhì)疏松癥的 相關(guān)性研究[J].中醫(yī)正骨,2012,24(04):16.
　CHEN Jun-jie*,LI Qing-qing,XIA Rong.*.Study on the correlations between the levels of lipid metabolism and serum visfatin and postmenopausal osteoporosis[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2012,24(06):16.

備注/Memo

備注/Memo:
基金項(xiàng)目:廣東省基礎(chǔ)與應(yīng)用基礎(chǔ)研究基金項(xiàng)目(2019A1515110723) 通訊作者:周琳 E-mail:[email protected]
更新日期/Last Update: 1900-01-01