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]馬靖哲,康武林,姚彬,等.蠲痹方含藥血清對(duì)絕經(jīng)后膝骨關(guān)節(jié)炎大鼠軟骨細(xì)胞自噬的影響及其作用機(jī)制[J].中醫(yī)正骨,2024,36(02):7-16.
　MA Jingzhe,KANG Wulin,YAO Bin,et al.Effects and mechanism of Juanbi Fang(蠲痹方)medicated serum on autophagy of chondrocytes in postmenopausal rats with knee osteoarthritis:an experimental study[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2024,36(02):7-16.
點(diǎn)擊復(fù)制

蠲痹方含藥血清對(duì)絕經(jīng)后膝骨關(guān)節(jié)炎大鼠軟骨細(xì)胞自噬的影響及其作用機(jī)制()
分享到：

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

卷:
第36卷
期數(shù):
2024年02期
頁(yè)碼:
7-16
欄目:
基礎(chǔ)研究
出版日期:
2024-02-20

文章信息/Info

Title:
Effects and mechanism of Juanbi Fang(蠲痹方)medicated serum on autophagy of chondrocytes in postmenopausal rats with knee osteoarthritis:an experimental study
作者:
馬靖哲1; 康武林1; 姚彬1; 黃文博1; 李越1; 陳小林2; 李思聰1; 袁普衛(wèi)1
(1.陜西中醫(yī)藥大學(xué)附屬醫(yī)院,陜西 咸陽(yáng) 712046; 2.陜西中醫(yī)藥大學(xué)藥學(xué)院,陜西 咸陽(yáng) 712046)
Author(s):
MA Jingzhe1; KANG Wulin1; YAO Bin1; HUANG Wenbo1; LI Yue1; CHEN Xiaolin2; LI Sicong1; YUAN Puwei1
1.The Affiliated Hospital of Shaanxi University of Chinese Medicine,Xianyang 712046,Shaanxi,China 2.College of Pharmacy,Shaanxi University of Chinese medicine,Xianyang 712046,Shaanxi,China
關(guān)鍵詞:
骨關(guān)節(jié)炎; 膝;  絕經(jīng)后期;  軟骨細(xì)胞;  自吞噬;  蠲痹方;  大鼠
Keywords:
osteoarthritis; knee;  postmenopause;  chondrocytes;  autophagy;  Juanbi Fang;  rats
摘要:
目的:探討蠲痹方含藥血清對(duì)絕經(jīng)后膝骨關(guān)節(jié)炎(knee osteoarthritis,KOA)大鼠軟骨細(xì)胞自噬的影響及其作用機(jī)制。方法:①絕經(jīng)后KOA動(dòng)物模型的建造和蠲痹方含藥血清的制備。采用摘取大鼠卵巢,并切斷膝關(guān)節(jié)內(nèi)側(cè)副韌帶、前交叉韌帶,摘除膝關(guān)節(jié)內(nèi)側(cè)半月板的方法,建造絕經(jīng)后KOA大鼠模型。造模成功后,對(duì)模型大鼠進(jìn)行蠲痹方濃縮液灌胃,制備蠲痹方含藥血清。②大鼠軟骨細(xì)胞的提取。分別取正常大鼠和模型大鼠的膝關(guān)節(jié)軟骨分離、提取軟骨細(xì)胞。③蠲痹方含藥血清最佳作用濃度篩選。將模型大鼠軟骨細(xì)胞分為模型組及1.25%、2.5%、5%、10%、20%含藥血清組6組,除模型組外,其余各組分別加入相應(yīng)體積分?jǐn)?shù)的蠲痹方含藥血清干預(yù)24 h。檢測(cè)各組軟骨細(xì)胞的活力,篩選蠲痹方含藥血清最佳作用濃度。④蠲痹方含藥血清對(duì)大鼠軟骨細(xì)胞G蛋白耦聯(lián)受體30(G protein-coupled receptor 30,GPR30)表達(dá)影響的檢測(cè)。將模型大鼠軟骨細(xì)胞分為模型組及1.25%、2.5%、5%、10%含藥血清組,并取正常大鼠軟骨細(xì)胞設(shè)為空白組。除模型組和空白組外,其他各組軟骨細(xì)胞用相應(yīng)體積分?jǐn)?shù)的蠲痹方含藥血清干預(yù)24 h。檢測(cè)各組大鼠軟骨細(xì)胞GPR30的相對(duì)表達(dá)量。⑤蠲痹方含藥血清對(duì)大鼠軟骨細(xì)胞自噬相關(guān)蛋白表達(dá)和AMP活化蛋白激酶(AMP-activated protein kinase,AMPK)/哺乳動(dòng)物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)信號(hào)通路影響的檢測(cè)。將模型大鼠軟骨細(xì)胞分為模型組、含藥血清組、含藥血清+Compound C組、Compound C組,并取正常大鼠軟骨細(xì)胞設(shè)為空白組。除模型組和空白組外,含藥血清組、含藥血清+Compound C組、Compound C組分別用10%蠲痹方含藥血清、10%蠲痹方含藥血清+Compound C及Compound C干預(yù)24 h。檢測(cè)各組軟骨細(xì)胞中自噬相關(guān)蛋白微管相關(guān)蛋白輕鏈3β(microtubule-associated protein light chain 3 beta,MAPLC3β)、Beclin-1、p62,及AMPK/mTOR信號(hào)通路相關(guān)蛋白磷酸化AMP活化蛋白激酶(phosphorylated AMP-activated protein kinase,p-AMPK)、磷酸化哺乳動(dòng)物雷帕霉素靶蛋白(phosphorylated mammalian target of rapamycin,p-mTOR)的相對(duì)表達(dá)量。結(jié)果:①動(dòng)物模型鑒定結(jié)果。造模8周后,可見造模大鼠膝關(guān)節(jié)表面軟骨毛糙或缺損,關(guān)節(jié)間隙變窄,滑膜增生,絕經(jīng)后KOA大鼠模型造模成功。②軟骨細(xì)胞鑒定結(jié)果。甲苯胺藍(lán)染色及Ⅱ型膠原蛋白免疫熒光鑒定結(jié)果顯示,所提取的細(xì)胞符合軟骨細(xì)胞特征。③蠲痹方含藥血清最佳作用濃度篩選結(jié)果。5%、10%、20%含藥血清組細(xì)胞活力均高于1.25%、2.5%含藥血清組和模型組(LSD-t=6.767,P=0.003,LSD-t=7.666,P=0.002,LSD-t=5.091,P=0.007; LSD-t=5.080,P=0.007,LSD-t=6.690,P=0.003,LSD-t=3.433,P=0.027; LSD-t=7.590,P=0.002,LSD-t=8.200,P=0.001,LSD-t=6.031,P=0.004); 10%含藥血清組細(xì)胞活力高于5%含藥血清組和20%含藥血清組(LSD-t=3.204,P=0.033,LSD-t=4.671,P=0.010)。④蠲痹方含藥血清對(duì)大鼠軟骨細(xì)胞GPR30表達(dá)影響的檢測(cè)結(jié)果。模型組GPR30相對(duì)表達(dá)量低于空白組及5%、10%含藥血清組(LSD-t=5.695,P=0.005,LSD-t=5.400,P=0.006,LSD-t=9.006,P=0.001),5%、10%含藥血清組GPR30相對(duì)表達(dá)量均高于1.25%含藥血清組(LSD-t=2.782,P=0.049,LSD-t=4.473,P=0.011),10%含藥血清組GPR30相對(duì)表達(dá)量高于2.5%含藥血清組(LSD-t=4.544,P=0.011)。⑤蠲痹方含藥血清對(duì)大鼠軟骨細(xì)胞自噬相關(guān)蛋白表達(dá)影響的檢測(cè)結(jié)果。模型組、含藥血清+Compound C組、Compound C組MAPLC3β相對(duì)表達(dá)量均低于空白組、含藥血清組(LSD-t=6.855,P=0.002,LSD-t=8.675,P=0.001; LSD-t=5.096,P=0.007,LSD-t=5.931,P=0.004; LSD-t=5.560,P=0.005,LSD-t=5.354,P=0.006); 模型組、Compound C組MAPLC3β相對(duì)表達(dá)量均低于含藥血清+Compound C組(LSD-t=4.627,P=0.010,LSD-t=8.677,P=0.001)。模型組、Compound C組Beclin-1相對(duì)表達(dá)量低于空白組、含藥血清組、含藥血清+Compound C(LSD-t=12.912,P=0.000,LSD-t=7.401,P=0.002,LSD-t=5.360,P=0.006; LSD-t=2.950,P=0.042,LSD-t=5.484,P=0.005,LSD-t=3.903,P=0.018); 含藥血清+Compound C組Beclin-1相對(duì)表達(dá)量低于空白組(LSD-t=26.840,P=0.000)。含藥血清組、空白組p62相對(duì)表達(dá)量低于模型組、含藥血清+Compound C組、Compound C組(LSD-t=3.925,P=0.017,LSD-t=3.985,P=0.019,LSD-t=0.016,P=0.001; LSD-t=3.149,P=0.035,LSD-t=5.094,P=0.007,LSD-t=8.740,P=0.001),含藥血清+Compound C組p62相對(duì)表達(dá)量低于Compound C組(LSD-t=3.455,P=0.026)。⑥蠲痹方含藥血清對(duì)大鼠軟骨細(xì)胞AMPK/mTOR信號(hào)通路影響的檢測(cè)結(jié)果。含藥血清組p-AMPK相對(duì)表達(dá)量高于模型組、Compound C組(LSD-t=3.623,P=0.022,LSD-t=6.537,P=0.003),空白組p-AMPK相對(duì)表達(dá)量高于模型組、含藥血清+Compound C組、Compound C組(LSD-t=4.149,P=0.014,LSD-t=2.791,P=0.049,LSD-t=5.734,P=0.004),含藥血清+Compound C組p-AMPK相對(duì)表達(dá)量高于Compound C組(LSD-t=5.958,P=0.004)。空白組、含藥血清組、含藥血清+Compound C組p-mTOR相對(duì)表達(dá)量均低于模型組(LSD-t=8.722,P=0.001,LSD-t=8.849,P=0.001,LSD-t=5.558,P=0.005),含藥血清組、空白組p-mTOR相對(duì)表達(dá)量均低于含藥血清+Compound C組、Compound C組(LSD-t=4.201,P=0.014,LSD-t=10.030,P=0.001; LSD-t=4.879,P=0.008,LSD-t=9.782,P=0.001),含藥血清+Compound C組p-mTOR相對(duì)表達(dá)量低于Compound C組(LSD-t=6.934,P=0.002)。結(jié)論:蠲痹方含藥血清作用于絕經(jīng)后KOA大鼠軟骨細(xì)胞,可增加細(xì)胞活力,并通過上調(diào)MAPLC3β、Beclin-1的表達(dá)和抑制p62的表達(dá)增強(qiáng)細(xì)胞自噬能力; 其作用機(jī)制可能與促進(jìn)GPR30表達(dá),上調(diào)AMPK磷酸化水平,下調(diào)mTOR磷酸化水平,激活GPR30和AMPK/mTOR信號(hào)通路有關(guān)。
Abstract:
Objective:To observe the effects of Juanbi Fang(蠲痹方,JBF)medicated serum on autophagy of chondrocytes in postmenopausal rats with knee osteoarthritis(KOA),and to explore its mechanism.Methods:①Twenty rats were subjected to ovariectomy,transection of knee medial collateral ligament(MCL)and anterior cruciate ligament(ACL),followed by knee medial meniscectomy for inducing postmenopausal KOA.After successful modeling,15 model rats were intragastric administrated with JBF concentrate for making JBF medicated serum.②The normal rats and model rats were sacrificed and their knee cartilages were harvested for isolating and extracting chondrocytes.③The chondrocytes extracted from the model rats were divided into model group,1.25% medicated serum group,2.5% medicated serum group,5% medicated serum group,10% medicated serum group,and 20% medicated serum group.Except for the model group,the chondrocytes in the other groups were intervened with JBF medicated serum in their corresponding volume fraction for consecutive 24 hours.After the end of intervention,the viability of chondrocytes in each group was detected,and the optimal acting concentration of the JBF medicated serum was screened.④The chondrocytes extracted from the model rats were assigned into model group,1.25% medicated serum group,2.5% medicated serum group,5% medicated serum group,and 10% medicated serum group,and the chondrocytes from the normal rats were taken as blank group.Except for the model group and blank group,the chondrocytes in other 4 groups were intervened with JBF medicated serum in their corresponding volume fraction for consecutive 24 hours.After the end of intervention,the relative expression level of G protein-coupled receptor 30(GPR30)in chondrocytes was detected by using Western blotting assay.⑤The chondrocytes extracted from the model rats were divided into model group,medicated serum group,medicated serum+Compound C group,and Compound C group,and the chondrocytes from the normal rats were taken as blank group.Except for the model group and blank group,the chondrocytes in medicated serum group,medicated serum+Compound C group,and Compound C group were intervened with 10% JBF medicated serum,10% JBF medicated serum combined with Compound C,and Compound C,respectively,for consecutive 24 hours.After the end of intervention,the relative expression levels of autophagy-related protein microtubule-associated protein light chain 3 beta(MAPLC3β),Beclin-1 and p62,as well as the relative expression levels of AMP-activated protein kinase(AMPK)/mammalian target of rapamycin(mTOR)signaling pathway-related protein phosphorylated AMP-activated protein kinase(p-AMPK)and phosphorylated mammalian target of rapamycin(p-mTOR)in chondrocytes was detected by using Western blotting assay.Results:①Eight weeks after the modeling,the coarse or defective cartilage on the knee surface,narrowed joint space,and proliferated synovial membrane were observed in the model rats,which suggested the models were successfully built.②The primary cells were stained with toluidine blue,and the intracellular typeⅡcollagen was detected by immunofluorescence staining,the results showed that the extracted cells were indicated as chondrocytes.③The chondrocyte viability was higher in 5%,10%,and 20% medicated serum group compared to 1.25%,2.5% medicated serum group and model group(LSD-t=6.767,P=0.003,LSD-t=7.666,P=0.002,LSD-t=5.091,P=0.007; LSD-t=5.080,P=0.007,LSD-t=6.690,P=0.003,LSD-t=3.433,P=0.027; LSD-t=7.590,P=0.002,LSD-t=8.200,P=0.001,LSD-t=6.031,P=0.004),and was higher in 10% medicated serum group compared to 5% and 20% medicated serum group(LSD-t=3.204,P=0.033,LSD-t=4.671,P=0.010).④The relative expression level of GPR30 in chondrocytes was lower in model group compared to blank group,5%,and 10% medicated serum group(LSD-t=5.695,P=0.005,LSD-t=5.400,P=0.006,LSD-t=9.006,P=0.001),and was higher in 5% and 10% medicated serum group compared to 1.25% medicated serum group(LSD-t=2.782,P=0.049,LSD-t=4.473,P=0.011),and was higher in 10% medicated serum group compared to 2.5% medicated serum group(LSD-t=4.544,P=0.011).⑤The relative expression level of MAPLC3β was lower in model group,medicated serum+Compound C group,and Compound C group compared to blank group and medicated serum group(LSD-t=6.855,P=0.002,LSD-t=8.675,P=0.001; LSD-t=5.096,P=0.007,LSD-t=5.931,P=0.004; LSD-t=5.560,P=0.005,LSD-t=5.354,P=0.006),and was lower in model group and Compound C group compared to medicated serum+Compound C group(LSD-t=4.627,P=0.010,LSD-t=8.677,P=0.001).The relative expression level of Beclin-1 was lower in model group and Compound C group compared to blank group,medicated serum group,and medicated serum+Compound C group(LSD-t=12.912,P=0.000,LSD-t=7.401,P=0.002,LSD-t=5.360,P=0.006; LSD-t=2.950,P=0.042,LSD-t=5.484,P=0.005,LSD-t=3.903,P=0.018),and was lower in medicated serum+Compound C group compared to blank group(LSD-t=26.840,P=0.000).The relative expression level of p62 was lower in medicated serum group and blank group compared to model group,medicated serum+Compound C group,and Compound C group(LSD-t=3.925,P=0.017,LSD-t=3.985,P=0.019,LSD-t=0.016,P=0.001; LSD-t=3.149,P=0.035,LSD-t=5.094,P=0.007,LSD-t=8.740,P=0.001),and was lower in medicated serum+Compound C group compared to Compound C group(LSD-t=3.455,P=0.026).⑥The relative expression level of p-AMPK was higher in medicated serum group compared to model group and Compound C group(LSD-t=3.623,P=0.022,LSD-t=6.537,P=0.003),and was higher in blank group compared to model group,medicated serum+Compound C group,and Compound C group(LSD-t=4.149,P=0.014,LSD-t=2.791,P=0.049,LSD-t=5.734,P=0.004),and was higher in medicated serum+Compound C group compared to Compound C group(LSD-t=5.958,P=0.004).The relative expression level of p-mTOR was lower in blank group,medicated serum group and medicated serum+Compound C group compared to model group(LSD-t=8.722,P=0.001,LSD-t=8.849,P=0.001,LSD-t=5.558,P=0.005),and was lower in medicated serum group and blank group compared to medicated serum+Compound C group and Compound C group(LSD-t=4.201,P=0.014,LSD-t=10.030,P=0.001; LSD-t=4.879,P=0.008,LSD-t=9.782,P=0.001),and was lower in medicated serum+Compound C group compared to Compound C group(LSD-t=6.934,P=0.002).Conclusion:JBF medicated serum can increase the viability of chondrocytes and enhance the autophagy ability of chondrocytes via up-regulating the expression of MAPLC3β and Beclin-1 and inhibiting the expression of p62 in postmenopausal rats with KOA.It may work by promoting the expression of GPR30,up-regulating the phosphorylation level of AMPK,down-regulating the phosphorylation level of mTOR,and activating signaling pathways of GPR30 and AMPK/mTOR.

參考文獻(xiàn)/References:

[1] HUNTER D J,BIERMA-ZEINSTRA S.Osteoarthritis[J].Lancet,2019,393: 1745-1759.
[2] SOFAT N.Analysing the role of endogenous matrix molecules in the development of osteoarthritis[J].Int J Exp Pathol,2009,90(5):463-479.
[3] PRIMORAC D,MOLNAR V,ROD E,et al.Knee Osteoarthritis:a review of pathogenesis and state-of-the-art non-operative therapeutic considerations[J]. Genes(Basel),2020,11(8):854.
[4] LOESER R F,GOLDRING S R,SCANZELLO C R,et al.Osteoarthritis:a disease of the joint as an organ[J]. Arthritis Rheum,2012,64(6):1697-1707.
[5] 王歡,孫賀,張耀南,等.中國(guó)40歲以上人群原發(fā)性膝骨關(guān)節(jié)炎各間室患病狀況調(diào)查[J].中華骨與關(guān)節(jié)外科雜志,2019,12(7):528-532.
[6] SRIKANTH V K,FRYER J L,ZHAI G,et al.A meta-analysis of sex differences prevalence,incidence and severity of osteoarthritis[J].Osteoarthritis Cartilage,2005,13(9):769-781.
[7] CHARLIER E,DEROYER C,CIREGIA F,et al.Chondrocyte dedifferentiation and osteoarthritis(OA)[J].Biochem Pharmacol,2019,165:49-65.
[8] FAVERO M,BELLUZZI E,TRISOLINO G,et al.Inflammatory molecules produced by meniscus and synovium in early and end-stage osteoarthritis:a coculture study[J].J Cell Physiol,2019,234(7):11176-11187.
[9] MOBASHERI A,RAYMAN M P,GUALILLO O,et al.The role of metabolism in the pathogenesis of osteoarthritis [J].Nat Rev Rheumatol,2017,13(5):302-311.
[10] KLIONSKY D J,ABDALLA F C,ABELIOVICH H,et al.Guidelines for the use and interpretation of assays for monitoring autophagy[J].Autophagy,2012,8(4):445-544.
[11] SHAPIRO I M,LAYFIELD R,LOTZ M,et al.Boning up on autophagy:the role of autophagy in skeletal biology[J].Autophagy,2014,10(1):7-19.
[12] 王軍威,朱添,郭小蘭,等.關(guān)節(jié)鏡手術(shù)聯(lián)合蠲痹膠囊治療膝骨性關(guān)節(jié)炎[J].長(zhǎng)春中醫(yī)藥大學(xué)學(xué)報(bào),2019,35(4):693-696.
[13] 楚向東,李玥.關(guān)節(jié)鏡結(jié)合內(nèi)服蠲痹膠囊為主治療膝骨關(guān)節(jié)炎的臨床觀察[J].陜西中醫(yī),2015,36(8):995-997.
[14] 袁普衛(wèi),李小群,康武林,等.蠲痹膠囊對(duì)膝骨關(guān)節(jié)炎豚鼠關(guān)節(jié)軟骨組織形態(tài)及滑膜中Toll樣受體4、NF-κB p65及腫瘤壞死因子-α表達(dá)的影響[J].中醫(yī)正骨,2016,28(9):5-12.
[15] 劉獻(xiàn)祥,李西海,周江濤.改良Hulth造模法復(fù)制膝骨性關(guān)節(jié)炎的實(shí)驗(yàn)研究[J].中國(guó)中西醫(yī)結(jié)合雜志,2005,25(12):1104-1108.
[16] 黃繼漢,黃曉暉,陳志揚(yáng),等.藥理試驗(yàn)中動(dòng)物間和動(dòng)物與人體間的等效劑量換算[J].中國(guó)臨床藥理學(xué)與治療學(xué),2004,9(9):1069-1072.
[17] 許學(xué)猛,劉文剛,許樹柴,等.膝骨關(guān)節(jié)炎(膝痹)中西醫(yī)結(jié)合臨床實(shí)踐指南[J].實(shí)用醫(yī)學(xué)雜志,2021,37(22):2827-2833.
[18] 胡興律,馮偉,袁普衛(wèi),等.蠲痹膠囊治療早期膝骨性關(guān)節(jié)炎45例臨床觀察[J].中國(guó)民族民間醫(yī)藥,2014,23(21):43-44.
[19] 成冬,郭磊,姜天龍,等.17β-雌二醇通過GPR30和PI3K/Akt信號(hào)通路影響ATDC5軟骨細(xì)胞線粒體自噬的機(jī)制[J].中國(guó)醫(yī)科大學(xué)學(xué)報(bào),2019,48(4):289-294.
[20] LI M,ZHANG L,LIU Z,et al.Sanse powder essential oil nanoemulsion negatively regulates trpa1 by ampk/mtor signaling in synovitis:knee osteoarthritis rat model and fibroblast-like synoviocyte isolates[J].Mediators Inflamm,2021,2021:4736670.
[21] DONG J,ZHANG J, LI G C,et al.CDDO-Im ameliorates osteoarthritis and inhibits chondrocyte apoptosis in mice via enhancing Nrf2-dependent autophagy[J].Acta Pharmacol Sin,2022,43(7):1793-1802.
[22] VALENTI M T,DALLE CARBONARE L,ZIPETO D,et al.Control of the autophagy pathway in osteoarthritis:key regulators,therapeutic targets and therapeutic strategies[J].Int J Mol Sci,2021,22(5):2700.
[23] LUO P,GAO F,NIU D,et al.The role of autophagy in chondrocyte metabolism and osteoarthritis:a comprehensive research review[J].Biomed Res Int,2019,2019:5171602.
[24] SHIMODA M,ODA S,SHIBATA M,et al.Change in regional cerebral blood flow following glycerol administration predicts.Clinical result from shunting in normal pressure hydrocephalus[J]. Acta Neurochir(Wien),1994,129(3/4):171-176.
[25] YAN Y,ZHOU XE,XU H E,et al.Structure and physiological regulation of AMPK[J].Int J Mol Sci,2018,19(11):3534.
[26] YAO Q,WU X,TAO C,et al.Osteoarthritis:pathogenic signaling pathways and therapeutic targets[J].Signal Transduct Target Ther,2023,8(1):56.
[27] SAXTON R A,SABATINI D M.mTOR signaling in growth,metabolism,and disease[J].Cell,2017,169(2):361-371.
[28] SARBASSOV D D,GUERTIN D A,ALI S M,et al.Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex[J]. Science,2005,307(5712):1098-1101.
[29] CARAMéS B,HASEGAWA A,TANIGUCHI N,et al.Autophagy activation by rapamycin reduces severity of experimental osteoarthritis[J].Ann Rheum Dis,2012,71(4):575-581.
[30] LEIDAL A M,LEVINE B,DEBNATH J.Autophagy and the cell biology of age-related disease[J].Nat Cell Biol,2018,20(12):1338-1348.
[31] LI Z,LIU L,YANG Y,et al.Metformin ameliorates sene-scence of adipose-derived mesenchymal stem cells and attenuates osteoarthritis progression via the ampk-dependent autophagy pathway[J].Oxid Med Cell Longev,2022,2022:4620254.

相似文獻(xiàn)/References:

[1]樊慶陽(yáng),任凱晶.定制3D打印切模輔助全膝關(guān)節(jié)置換術(shù)治療 膝骨關(guān)節(jié)炎合并股骨干骨折畸形愈合[J].中醫(yī)正骨,2015,27(11):37.
[2]劉曉雅,孫永強(qiáng),劉國(guó)杰.主動(dòng)快速康復(fù)鍛煉對(duì)全膝關(guān)節(jié)置換術(shù)后關(guān)節(jié)活動(dòng)度的影響[J].中醫(yī)正骨,2015,27(09):73.
[3]鄭春松,葉蕻芝,李西海,等.透骨消痛膠囊中補(bǔ)腎柔肝藥和活血祛風(fēng)藥治療 骨關(guān)節(jié)炎作用方式的計(jì)算機(jī)模擬比較[J].中醫(yī)正骨,2015,27(07):6.
　ZHENG Chunsong,YE Hongzhi,LI Xihai,et al.Comparison of the mode of action of Bushen Rougan(補(bǔ)腎柔肝)drugs versus Huoxue Qufeng(活血祛風(fēng))drugs contained in Tougu Xiaotong Jiaonang(透骨消痛膠囊)for the treatment of osteoarthritis:A computer simulation study[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2015,27(02):6.
[4]宋兵華,孫俊英,倪增良,等.全膝關(guān)節(jié)置換術(shù)前CT測(cè)量股骨后髁角的臨床意義[J].中醫(yī)正骨,2015,27(07):38.
[5]鄭春松,葉蕻芝,李西海,等.獨(dú)活寄生湯含藥血清對(duì)白細(xì)胞介素1β誘導(dǎo)的 退變關(guān)節(jié)軟骨細(xì)胞中基質(zhì)金屬蛋白酶 和環(huán)氧化酶2表達(dá)的影響[J].中醫(yī)正骨,2015,27(12):1.
　ZHENG Chunsong,YE Hongzhi,LI Xihai,et al.Impact of Duhuo Jisheng Tang(獨(dú)活寄生湯)medicated serum on expression of matrix metalloproteinase and cyclooxygenase 2 in degenerative articular chondrocytes induced by interleukin-1 beta[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2015,27(02):1.
[6]王金良,孫京濤,李玲,等.骨水泥聯(lián)合螺釘修復(fù)全膝關(guān)節(jié)置換術(shù)中 脛骨平臺(tái)內(nèi)側(cè)骨缺損[J].中醫(yī)正骨,2015,27(12):55.
[7]馮榮,王平,李炳奇,等.鈹針刺絡(luò)拔罐結(jié)合中藥口服治療膝骨關(guān)節(jié)炎合并 原發(fā)性血小板增多癥1例[J].中醫(yī)正骨,2015,27(12):73.
[8]蔡云仙.圍手術(shù)期耳穴按壓聯(lián)合平衡針療法 在全膝關(guān)節(jié)置換術(shù)后鎮(zhèn)痛中的應(yīng)用[J].中醫(yī)正骨,2015,27(06):41.
[9]張榮,王健.人工全膝關(guān)節(jié)置換術(shù)的圍手術(shù)期心理護(hù)理[J].中醫(yī)正骨,2015,27(05):77.
[10]喻長(zhǎng)純,楊明路,王戰(zhàn)朝.不同手術(shù)方式治療脛骨平臺(tái)骨折畸形愈合的體會(huì)[J].中醫(yī)正骨,2015,27(03):37.
[11]孟維娜,明立功,王新德,等.關(guān)節(jié)鏡下清理聯(lián)合腓骨近1/3段截骨治療膝骨關(guān)節(jié)炎[J].中醫(yī)正骨,2015,27(11):40.
[12]明立功,孟維娜,王新德,等.腓骨近端截骨治療內(nèi)側(cè)間室膝骨關(guān)節(jié)炎的近期療效觀察[J].中醫(yī)正骨,2015,27(10):25.
[13]張杰,王人彥,張玉柱.膝骨關(guān)節(jié)炎的治療進(jìn)展[J].中醫(yī)正骨,2015,27(10):68.
[14]梁朝,蔡靜怡,閆立,等.針刀療法改善膝骨關(guān)節(jié)炎早期疼痛癥狀的療效評(píng)價(jià)[J].中醫(yī)正骨,2015,27(09):9.
　LIANG Zhao,CAI Jingyi,YAN Li,et al.Evaluation of the curative effect of needle-knife therapy for relieving knee pain in patients with early knee osteoarthritis[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2015,27(02):9.
[15]王建武,黨建軍,李強(qiáng),等.四聯(lián)療法治療膝骨關(guān)節(jié)炎[J].中醫(yī)正骨,2015,27(08):44.
[16]劉紅娟,郭會(huì)利,郭樹農(nóng).云克聯(lián)合中藥治療膝骨關(guān)節(jié)炎的護(hù)理[J].中醫(yī)正骨,2015,27(08):75.
[17]陳衛(wèi)衡.探索建立系統(tǒng)的膝骨關(guān)節(jié)炎中醫(yī)臨床科研范式 和理論體系[J].中醫(yī)正骨,2015,27(07):1.
[18]帥波,沈霖,楊艷萍,等.加味青娥丸治療膝骨關(guān)節(jié)炎的作用機(jī)制研究[J].中醫(yī)正骨,2015,27(07):15.
　SHUAI Bo,SHEN Lin,YANG Yanping,et al.Study on the mechanism of action of Jiawei Qing'e Wan(加味青娥丸)for the treatment of knee osteoarthritis[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2015,27(02):15.
[19]梅其杰,袁長(zhǎng)深,段戡,等.壯藥骨痹方燙熨聯(lián)合運(yùn)動(dòng)療法治療膝骨關(guān)節(jié)炎的臨床研究[J].中醫(yī)正骨,2015,27(07):27.
　MEI Qijie,YUAN Changshen,DUAN Kan,et al.Clinical study of the curative effect of hot compressing and rubbing with packet of Gubi Fang(骨痹方)combined with exercise therapy in the treatment of knee osteoarthritis[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2015,27(02):27.
[20]王丹輝,張燕,劉麗娟,等.重組人Ⅱ型腫瘤壞死因子受體-抗體融合蛋白 關(guān)節(jié)腔注射聯(lián)合中藥薰洗治療膝骨關(guān)節(jié)炎的臨床研究[J].中醫(yī)正骨,2015,27(07):31.
　WANG Danhui,ZHANG Yan,LIU Lijuan,et al.Clinical study on intra-articular injection of TypeⅡrecombinant human tumor necrosis factor receptor-Fc fusion protein combined with Chinese herbal steaming and washing therapy for treatment of knee osteoarthritis[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2015,27(02):31.

備注/Memo

備注/Memo:
基金項(xiàng)目:陜西省教育廳青年創(chuàng)新團(tuán)隊(duì)建設(shè)科研計(jì)劃項(xiàng)目(21JP035); 陜西省教育廳服務(wù)地方專項(xiàng)計(jì)劃項(xiàng)目(21JC010); 咸陽(yáng)市重點(diǎn)研發(fā)計(jì)劃項(xiàng)目(2019k01-53)
通訊作者:袁普衛(wèi) E-mail:[email protected]
更新日期/Last Update: 1900-01-01