[1]林琳,梁伟财.LINC00847调控miR-100-5p-卷曲蛋白8调控轴对骨关节炎软骨细胞的影响及其作用机制[J].中医正骨,2026,38(03):8-21.
　LIN Lin,LIANG Weicai.Effects of LINC00847 regulating miR-100-5p-frizzled protein 8 regulatory axis on osteoarthritis chondrocytes and its mechanism of action[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2026,38(03):8-21.
点击复制

LINC00847调控miR-100-5p-卷曲蛋白8调控轴对骨关节炎软骨细胞的影响及其作用机制()

《中医正骨》[ISSN:1001-6015/CN:41-1162/R]

卷:
第38卷
期数:
2026年03期
页码:
8-21
栏目:
基础研究
出版日期:
2026-03-20

文章信息/Info

Title:
Effects of LINC00847 regulating miR-100-5p-frizzled protein 8 regulatory axis on osteoarthritis chondrocytes and its mechanism of action
作者:
林琳; 梁伟财
(南方医科大学第八附属医院/佛山市顺德区第一人民医院,广东 佛山 528300)
Author(s):
LIN Lin; LIANG Weicai
The Eighth Affiliated Hospital of Southern Medical University(The First People's Hospital of Shunde),Foshan 528300,Guangdong,China
关键词:
骨关节炎;  软骨细胞;  LINC00847;  miR-100-5p;  卷曲蛋白8;  细胞凋亡;  细胞增殖;  炎症
Keywords:
osteoarthritis;  chondrocytes;  LINC00847;  miR-100-5p;  frizzled protein 8;  apoptosis;  cell proliferation;  inflammation
摘要:
目的:探究LINC00847调控miR-100-5p-卷曲蛋白8(frizzled protein 8,FZD8)调控轴对骨关节炎软骨细胞的影响及其作用机制。方法:①miR-100-5p与LINC00847预测靶位点结合的验证方法。取处于对数生长期的软骨细胞,分为阴性对照组和miR-100-5p过表达组,每组6个复孔,每组的1～3号孔为野生型LINC00847亚组,4～6号孔为突变型LINC00847亚组。阴性对照组的野生型LINC00847亚组转染miR-100-5p模拟物阴性对照物和野生型LINC00847 pmirGLO重组载体,突变型LINC00847亚组转染miR-100-5p模拟物阴性对照物和突变型LINC00847 pmirGLO重组载体; miR-100-5p过表达组的野生型LINC00847亚组转染miR-100-5p模拟物和野生型LINC00847 pmirGLO重组载体,突变型LINC00847亚组转染miR-100-5p模拟物和突变型LINC00847 pmirGLO重组载体。培养48 h后,收集各组软骨细胞检测相对萤光素酶活性。②miR-100-5p与FZD8预测靶位点结合的验证方法。采用与①相同的方法进行miR-100-5p与FZD8预测靶位点结合的验证,仅将野生型LINC00847 pmirGLO重组载体换为野生型FZD8 pmirGLO重组载体,将突变型LINC00847 pmirGLO重组载体换为突变型FZD8 pmirGLO重组载体。③敲低LINC00847对骨关节炎软骨细胞影响的分析方法。取处于对数生长期的软骨细胞,分为LINC00847敲低阴性对照组和LINC00847敲低组。LINC00847敲低阴性对照组和LINC00847敲低组分别转染非靶向干扰小RNA(small interfering RNA,siRNA)和靶向LINC00847的siRNA。确定转染成功后,将各组软骨细胞置于含10 ng·mL-1白细胞介素(interleukin,IL)-1β的培养基中,培养24 h后检测各组软骨细胞的存活率、凋亡率、培养基上清液中促炎性细胞因子含量,LINC00847、miR-100-5p、FZD8 mRNA的表达水平,以及FZD8、抗增殖细胞核抗原(proliferating cell nuclear antigen,PCNA)、Ki67、B淋巴细胞瘤-2(B-cell lymphoma-2,Bcl-2)、B淋巴细胞瘤-2相关X蛋白(B-cell lymphoma-2 associated X protein,Bax)、β联蛋白、Ⅱ型胶原蛋白α1链(collagen type Ⅱα1,COL2A1)、基质金属蛋白酶(matrix metalloproteinase,MMP)-13的蛋白表达水平。④过表达LINC00847对骨关节炎软骨细胞影响的分析方法。取处于对数生长期的软骨细胞,分为LINC00847过表达阴性对照组和LINC00847过表达组。LINC00847过表达阴性对照组和LINC00847过表达组分别转染pcDNA3.1空载体和pcDNA3.1 LINC00847重组载体。确定转染成功后,将各组软骨细胞置于含10 ng·mL-1 IL-1β的培养基中,培养24 h后检测③中各项指标。⑤过表达LINC00847和miR-100-5p对骨关节炎软骨细胞影响的分析方法。取处于对数生长期的软骨细胞,分为miR-100-5p过表达阴性对照组、LINC00847和miR-100-5p过表达组。miR-100-5p过表达阴性对照组转染pcDNA3.1 LINC00847重组载体和miR-100-5p模拟物阴性对照物,LINC00847和miR-100-5p过表达组转染pcDNA3.1 LINC00847重组载体和miR-100-5p模拟物。确定转染成功后,将各组软骨细胞置于含10 ng·mL-1 IL-1β的培养基中,培养24 h后检测③中除LINC00847外的各项指标。⑥过表达LINC00847、miR-100-5p和FZD8对骨关节炎软骨细胞影响的分析方法。取处于对数生长期的软骨细胞,分为FZD8过表达阴性对照组及LINC00847、miR-100-5p和FZD8过表达组。FZD8过表达阴性对照组转染pcDNA3.1 LINC00847重组载体、miR-100-5p模拟物和pcDNA3.1空载体,LINC00847、miR-100-5p和FZD8过表达组转染pcDNA3.1 LINC00847重组载体、miR-100-5p模拟物、pcDNA3.1 FZD8重组载体。确定转染成功后,将各组软骨细胞置于含10 ng·mL-1 IL-1β的培养基中,培养24 h后检测③中除LINC00847、miR-100-5p外的各项指标。结果:①miR-100-5p与LINC00847预测靶位点结合的验证结果。miR-100-5p过表达组的野生型LINC00847亚组软骨细胞的相对萤光素酶活性低于阴性对照组的野生型LINC00847亚组(t=8.521,P=0.000),miR-100-5p过表达组的突变型LINC00847亚组软骨细胞的相对萤光素酶活性与阴性对照组的突变型LINC00847亚组的差异无统计学意义(t=0.326,P=0.758)。②miR-100-5p与FZD8预测靶位点结合的验证结果。miR-100-5p过表达组的野生型FZD8亚组软骨细胞的相对萤光素酶活性低于阴性对照组的野生型FZD8亚组(t=10.376,P=0.000),miR-100-5p过表达组的突变型FZD8亚组软骨细胞的相对萤光素酶活性与阴性对照组的突变型FZD8亚组的差异无统计学意义(t=0.408,P=0.700)。③敲低LINC00847对骨关节炎软骨细胞影响的分析结果。LINC00847敲低组软骨细胞的存活率高于LINC00847敲低阴性对照组(t=3.723,P=0.014),凋亡率低于LINC00847敲低阴性对照组(t=7.437,P=0.001); LINC00847敲低组软骨细胞培养基上清液中TNF-α、IL-6含量均低于LINC00847敲低阴性对照组(t=14.303,P=0.000; t=16.383,P=0.000),IL-10含量高于LINC00847敲低阴性对照组(t=12.576,P=0.000); LINC00847敲低组软骨细胞中LINC00847、FZD8 mRNA的表达水平均低于LINC00847敲低阴性对照组(t=19.290,P=0.000; t=12.135,P=0.000),miR-100-5p的表达水平高于LINC00847敲低阴性对照组(t=5.593,P=0.003); LINC00847敲低组软骨细胞中FZD8、Bax、β联蛋白、MMP-13蛋白表达水平均低于LINC00847敲低阴性对照组(t=7.097,P=0.001; t=7.668,P=0.000; t=14.330,P=0.000; t=10.844,P=0.000),PCNA、Ki67、Bcl-2、COL2A1蛋白表达水平均高于LINC00847敲低阴性对照组(t=9.102,P=0.000; t=9.295,P=0.000; t=7.129,P=0.001; t=9.327,P=0.000)。④过表达LINC00847对骨关节炎软骨细胞影响的分析结果。LINC00847过表达组软骨细胞的存活率低于LINC00847过表达阴性对照组(t=3.200,P=0.024),凋亡率高于LINC00847过表达阴性对照组(t=14.363,P=0.000); LINC00847过表达组软骨细胞培养基上清液中TNF-α、IL-6含量均高于LINC00847过表达阴性对照组(t=7.117,P=0.001; t=4.904,P=0.004),IL-10含量低于LINC00847过表达阴性对照组(t=11.376,P=0.000); LINC00847过表达组软骨细胞中LINC00847、FZD8 mRNA的表达水平均高于LINC00847过表达阴性对照组(t=9.129,P=0.000; t=7.703,P=0.001),miR-100-5p的表达水平低于LINC00847过表达阴性对照组(t=4.654,P=0.006); LINC00847过表达组软骨细胞中FZD8、Bax、β联蛋白、MMP-13蛋白表达水平均高于LINC00847过表达阴性对照组(t=5.809,P=0.002; t=5.765,P=0.002; t=5.284,P=0.003; t=11.900,P=0.000),PCNA、Ki67、Bcl-2、COL2A1蛋白表达水平均低于LINC00847过表达阴性对照组(t=7.723,P=0.001; t=5.765,P=0.002; t=9.127,P=0.000; t=12.394,P=0.000)。⑤过表达LINC00847和miR-100-5p对骨关节炎软骨细胞影响的分析结果。LINC00847和miR-100-5p过表达组软骨细胞的存活率高于miR-100-5p过表达阴性对照组(t=5.756,P=0.002),凋亡率低于miR-100-5p过表达阴性对照组(t=15.060,P=0.000); LINC00847和miR-100-5p过表达组软骨细胞培养基上清液中TNF-α、IL-6含量均低于miR-100-5p过表达阴性对照组(t=5.725,P=0.002; t=5.063,P=0.004),IL-10含量高于miR-100-5p过表达阴性对照组(t=11.090,P=0.000); LINC00847和miR-100-5p过表达组软骨细胞中miR-100-5p的表达水平高于miR-100-5p过表达阴性对照组(t=7.929,P=0.001),FZD8 mRNA的表达水平低于miR-100-5p过表达阴性对照组(t=7.984,P=0.001); LINC00847和miR-100-5p过表达组软骨细胞中FZD8、Bax、β联蛋白、MMP-13蛋白表达水平均低于miR-100-5p过表达阴性对照组(t=6.005,P=0.002; t=7.206,P=0.001; t=5.101,P=0.004; t=9.505,P=0.000),PCNA、Ki67、Bcl-2、COL2A1蛋白表达水平均高于miR-100-5p过表达阴性对照组(t=9.353,P=0.000; t=10.392,P=0.000; t=8.573,P=0.000; t=7.668,P=0.001)。⑥过表达LINC00847、miR-100-5p和FZD8对骨关节炎软骨细胞影响的分析结果。LINC00847、miR-100-5p和FZD8过表达组软骨细胞的存活率低于FZD8过表达阴性对照组(t=4.673,P=0.006),凋亡率高于FZD8过表达阴性对照组(t=3.444,P=0.018); LINC00847、miR-100-5p和FZD8过表达组软骨细胞培养基上清液中TNF-α、IL-6含量均高于FZD8过表达阴性对照组(t=5.419,P=0.003; t=3.384,P=0.020),IL-10含量低于FZD8过表达阴性对照组(t=7.964,P=0.001); LINC00847、miR-100-5p和FZD8过表达组软骨细胞中FZD8 mRNA的表达水平高于FZD8过表达阴性对照组(t=8.487,P=0.000); LINC00847、miR-100-5p和FZD8过表达组软骨细胞中FZD8、Bax、β联蛋白、MMP-13蛋白表达水平均高于FZD8过表达阴性对照组(t=2.882,P=0.034; t=6.725,P=0.001; t=3.548,P=0.016; t=7.621,P=0.001),PCNA、Ki67、Bcl-2、COL2A1蛋白表达水平均低于FZD8过表达阴性对照组(t=9.208,P=0.000; t=8.317,P=0.000; t=8.647,P=0.000; t=6.245,P=0.002)。结论:LINC00847能够通过调控miR-100-5p-FZD8调控轴影响骨关节炎软骨细胞的增殖、凋亡、炎症反应和细胞外基质降解,其具体作用机制为LINC00847过表达能够下调miR-100-5p表达水平,上调FZD8表达水平,进而抑制骨关节软骨细胞的增殖,促进其凋亡、炎症反应和细胞外基质降解。
Abstract:
Objective:To investigate the effects of LINC00847 on osteoarthritis(OA)chondrocytes via regulating the miR-100-5p-frizzled protein 8(FZD8)regulatory axis,and to explore its underlying mechanism.Methods:①Validation method for the binding of miR-100-5p to the predicted target site of LINC00847.Chondrocytes in the logarithmic growth phase were collected and divided into a negative control group and a miR-100-5p overexpression group,with 6 replicate wells in each group.Wells 1–3 in each group served as the wild-type LINC00847 subgroup,while wells 4-6 as the mutant LINC00847 subgroup.In the negative control group,the wild-type LINC00847 subgroup was co-transfected with miR-100-5p mimic negative control and wild-type LINC00847 pmirGLO recombinant vector,while the mutant LINC00847 subgroup with miR-100-5p mimic negative control and mutant LINC00847 pmirGLO recombinant vector.In the miR-100-5p overexpression group,the wild-type LINC00847 subgroup was co-transfected with miR-100-5p mimic and wild-type LINC00847 pmirGLO recombinant vector,while the mutant LINC00847 subgroup with miR-100-5p mimic and mutant LINC00847 pmirGLO recombinant vector.After 48-hour culture,the transfected chondrocytes were collected from each group to detect the relative luciferase activity.②Validation method for the binding of miR-100-5p to the predicted target site of FZD8.The same procedure as described in item ① was followed to validate the binding between miR-100-5p and the predicted target site of FZD8,only substituting the wild-type LINC00847 pmirGLO recombinant vector with the wild-type FZD8 pmirGLO recombinant vector,and the mutant LINC00847 pmirGLO recombinant vector with the mutant FZD8 pmirGLO recombinant vector.③Analysis method for the effects of LINC00847 knockdown on OA chondrocytes.Chondrocytes in the logarithmic growth phase were selected and divided into a LINC00847 knockdown negative control group and a LINC00847 knockdown group,and transfected with non-targeting small interfering RNA(siRNA)and LINC00847-targeting siRNA,respectively.Following the successful transfection,chondrocytes in each group were cultured in medium containing 10 ng/mL interleukin(IL)-1β.After 24-hour culture,the survival rate and apoptosis rate of chondrocytes,the pro-inflammatory cytokine levels in the culture supernatant,the mRNA expression levels of LINC00847,miR-100-5p,and FZD8,as well as the protein expression levels of FZD8,proliferating cell nuclear antigen(PCNA),Ki67,B-cell lymphoma-2(Bcl-2),B-cell lymphoma-2 associated X protein(Bax),β-catenin,collagen type Ⅱα1(COL2A1),and matrix metalloproteinase(MMP)-13 were detected in each group.④Analysis method for the effects of LINC00847 overexpression on OA chondrocytes.Chondrocytes in the logarithmic growth phase were selected and divided into a LINC00847 overexpression negative control group and a LINC00847 overexpression group,and transfected with pcDNA3.1 empty vector and pcDNA3.1 LINC00847 recombinant vector,respectively.Following the successful transfection,chondrocytes in each group were cultured in medium containing 10 ng/mL IL-1β for 24 hours.After 24-hour culture,the indicators as described in item ③ were detected.⑤Analysis method for the effects of combined LINC00847 and miR-100-5p overexpression on OA chondrocytes.Chondrocytes in the logarithmic growth phase were selected and divided into a miR-100-5p overexpression negative control group and a combined LINC00847 and miR-100-5p overexpression group.The former group was co-transfec-ted with pcDNA3.1 LINC00847 recombinant vector and miR-100-5p mimic negative control,while the latter group with pcDNA3.1 LINC00847 recombinant vector and miR-100-5p mimic.Following the successful transfection,chondrocytes in each group were cultured in medium containing 10 ng/mL IL-1β for 24 hours.After 24-hour culture,the same indicators as described in item ③,except LINC00847,were detected.⑥Analysis method for the effects of combined LINC00847,miR-100-5p,and FZD8 overexpression on OA chondrocytes.Chondrocytes in the logarithmic growth phase were selected and divided into a FZD8 overexpression negative control group and a combined LINC00847,miR-100-5p,and FZD8 overexpression group.The former group was co-transfected with pcDNA3.1 LINC00847 recombinant vector,miR-100-5p mimic,and pcDNA3.1 empty vector,while the latter group with pcDNA3.1 LINC00847 recombinant vector,miR-100-5p mimic,and pcDNA3.1 FZD8 recombinant vector.Following the successful transfection,chondrocytes in each group were cultured in medium containing 10 ng/mL IL-1β for 24 hours.After 24-hour culture,the same indicators as described in item ③,except LINC00847 and miR-100-5p,were detected.Results:①Verification results of binding between miR-100-5p and the predicted target site of LINC00847.The relative luciferase activity of chondrocytes was significantly lower in the wild-type LINC00847 subgroup of the miR-100-5p overexpression group compared to the wild-type LINC00847 subgroup of the negative control group(t=8.521,P=0.000),while no significant difference was observed between the mutant LINC00847 subgroups of the two groups(t=0.326,P=0.758).②Verification results of binding between miR-100-5p and the predicted target site of FZD8.The relative luciferase activity of chondrocytes was significantly lower in the wild-type FZD8 subgroup of the miR-100-5p overexpression group compared to the wild-type FZD8 subgroup of the negative control group(t=10.376,P=0.000),while no significant difference was observed between the mutant FZD8 subgroups of the two groups(t=0.408,P=0.700).③The effects of LINC00847 knockdown on OA chondrocytes.The survival rate of chondrocytes(t=3.723,P=0.014),expression level of miR-100-5p in chondrocytes(t=5.593,P=0.003),and protein expression levels of PCNA,Ki67,Bcl-2,and COL2A1 in chondrocytes(t=9.102,P=0.000; t=9.295,P=0.000; t=7.129,P=0.001; t=9.327,P=0.000)increased,while the apoptosis rate of chondrocytes(t=7.437,P=0.001),mRNA expression levels of LINC00847 and FZD8 in chondrocytes(t=19.290,P=0.000; t=12.135,P=0.000),and protein expression levels of FZD8,Bax,β-catenin,and MMP-13 in chondrocytes(t=7.097,P=0.001; t=7.668,P=0.000; t=14.330,P=0.000; t=10.844,P=0.000)decreased in the LINC00847 knockdown group compared to the LINC00847 knockdown negative control group.In addition,the TNF-α and IL-6 levels in the culture supernatant were lower,while the IL-10 level was higher in the LINC00847 knockdown group compared to the LINC00847 knockdown negative control group(t=14.303,P=0.000; t=16.383,P=0.000; t=12.576,P=0.000).④The effects of LINC00847 overexpression on OA chondrocytes.The apoptosis rate of chondrocytes(t=14.363,P=0.000),mRNA expression levels of LINC00847 and FZD8 in chondrocytes(t=9.129,P=0.000; t=7.703,P=0.001),and protein expression levels of FZD8,Bax,β-catenin,and MMP-13 in chondrocytes(t=5.809,P=0.002; t=5.765,P=0.002; t=5.284,P=0.003; t=11.900,P=0.000)increased,while the survival rate of chondrocytes(t=3.200,P=0.024),expression level of miR-100-5p in chondrocytes(t=4.654,P=0.006),and protein expression levels of PCNA,Ki67,Bcl-2,and COL2A1 in chondrocytes(t=7.723,P=0.001; t=5.765,P=0.002; t=9.127,P=0.000; t=12.394,P=0.000)decreased in the LINC00847 overexpression group compared to the LINC00847 overexpression negative control group.In addition,the TNF-α and IL-6 levels in the culture supernatant were higher,while the IL-10 level was lower in the LINC00847 overexpression group compared to the LINC00847 overexpression negative control group(t=7.117,P=0.001; t=4.904,P=0.004; t=11.376,P=0.000).⑤Effects of combined LINC00847 and miR-100-5p overexpression on OA chondrocytes.The survival rate of chondrocytes(t=5.756,P=0.002),expression level of miR-100-5p in chondrocytes(t=7.929,P=0.001),and protein expression levels of PCNA,Ki67,Bcl-2,and COL2A1 in chondrocytes(t=9.353,P=0.000; t=10.392,P=0.000; t=8.573,P=0.000; t=7.668,P=0.001)increased,while the apoptosis rate of chondrocytes(t=15.060,P=0.000),mRNA expression level of FZD8 in chondrocytes(t=7.984,P=0.001),and protein expression levels of FZD8,Bax,β-catenin,and MMP-13 in chondrocytes(t=6.005,P=0.002; t=7.206,P=0.001; t=5.101,P=0.004; t=9.505,P=0.000)decreased in combined LINC00847 and miR-100-5p overexpression group compared to the miR-100-5p overexpression negative control group.In addition,the TNF-α and IL-6 levels in the culture supernatant were lower,while the IL-10 level was higher in combined LINC00847 and miR-100-5p overexpression group compared to the miR-100-5p overexpression negative control group(t=5.725,P=0.002; t=5.063,P=0.004; t=11.090,P=0.000).⑥Effects of combined LINC00847,miR-100-5p,and FZD8 overexpression on OA chondrocytes.The apoptosis rate of chondrocytes(t=3.444,P=0.018),mRNA expression level of FZD8 in chondrocytes(t=8.487,P=0.000),and protein expression levels of FZD8,Bax,β-catenin,and MMP-13 in chondrocytes(t=2.882,P=0.034; t=6.725,P=0.001; t=3.548,P=0.016; t=7.621,P=0.001)increased,while the survival rate of chondrocytes(t=4.673,P=0.006),and protein expression levels of PCNA,Ki67,Bcl-2,and COL2A1 in chondrocytes(t=9.208,P=0.000; t=8.317,P=0.000; t=8.647,P=0.000; t=6.245,P=0.002)decreased in combined LINC00847,miR-100-5p,and FZD8 overexpression group compared to FZD8 overexpression negative control group.In addition,the TNF-α and IL-6 levels in the culture supernatant were higher,while the IL-10 level was lower in combined LINC00847,miR-100-5p,and FZD8 overexpression group compared to FZD8 overexpression negative control group(t=5.419,P=0.003; t=3.384,P=0.020; t=7.964,P=0.001).Conclusion:LINC00847 can affect the proliferation,apoptosis,inflammatory response,and extracellular matrix degradation of OA chondrocytes by regulating the miR-100-5p-FZD8 regulatory axis.It may work by downregulating the expression level of miR-100-5p,and upregulating the expression level of FZD8 through overexpression of LINC00847,thereby inhibiting the proliferation of OA chondrocytes and promoting their apoptosis,inflammatory response,and extracellular matrix degradation.

参考文献/References:

[1] FUGGLE N,LASLOP A,RIZZOLI R,et al.Treatment of osteoporosis and osteoarthritis in the oldest old[J].Drugs,2025,85(3):343-360.
[2] CHEN H T,LIU S Y,XING J W,et al.Orientin alleviates chondrocyte senescence and osteoarthritis by inhibiting PI3K/AKT pathway[J].Bone Joint Res,2025,14(3):245-258.
[3] LIU J X,CHENG J Q,ZHOU H,et al.CRNDE alleviates IL-1β-induced chondrocyte damage by modulating miR-31/NF-κB pathway[J].J Orthop Surg Res,2024,19(1):860.
[4] LAI Z,CAO Y G.Plasma miR-200c-3p,miR-100-5p,and miR-1826 serve as potential diagnostic biomarkers for knee osteoarthritis:randomized controlled trials[J].Medicine(Baltimore),2019,98(51):e18110.
[5] LUO P,JIANG C,JI P,et al.Exosomes of stem cells from human exfoliated deciduous teeth as an anti-inflammatory agent in temporomandibular joint chondrocytes via miR-100-5p/mTOR[J].Stem Cell Res Ther,2019,10(1):216.
[6] 周婉婉.黄芩清热除痹胶囊通过FZD8-Wnt/β-catenin信号通路改善类风湿性关节炎的机制研究[D].合肥:安徽中医药大学,2023.
[7] LIU Y,WEI J,WANG C,et al.MicroRNA-543 controls pancreatic cancer development by LINC00847-microRNA-543-STK31 axis[J].J Gastrointest Oncol,2022,13(6):3263-3277.
[8] LI H,CHEN Y K,WAN Q,et al.Long non-coding RNA LINC00847 induced by E2F1 accelerates non-small cell lung cancer progression through targeting miR-147a/IFITM1 axis[J].Front Med(Lausanne),2021,8:663558.
[9] 于琪英.LINC00847通过Hsa-miR-100-5p/HOXA1轴调控胃癌转移机制的研究[D].武汉:武汉科技大学,2023.
[10] MA P,HAN J L.Overexpression of miR-100-5p inhibits pap-illary thyroid cancer progression via targeting FZD8[J].Open Med(Wars),2022,17(1):1172-1182.
[11] 胡子旋,姚楠,黄丹娥,等.补肾强筋胶囊含药血清对膝骨关节炎软骨细胞模型自噬影响的实验研究[J].中医正骨,2025,37(1):38-44.
[12] ZHANG Y,LI Z H,CHEN C,et al.S100A12 is involved in the pathology of osteoarthritis by promoting M1 macrophage polarization via the NF-κB pathway[J].Connect Tissue Res,2024,65(2):133-145.
[13] DONG S Y,LI X L,XU G R,et al.Quercetin attenuates the symptoms of osteoarthritis in vitro and in vivo by suppressing ferroptosis via activation of AMPK/Nrf2/Gpx4 signa-ling[J].Mol Med Rep,2025,31(3):60.
[14] ZHANG L,ZHANG P,SUN X Y,et al.Long non-coding RNA DANCR regulates proliferation and apoptosis of chondrocytes in osteoarthritis via miR-216a-5p-JAK2-STAT3 axis[J].Biosci Rep,2018,38(6):BSR20181228.
[15] LI H T,LIAN K H,MAO J G,et al.LncRNA LEMD1-AS1 relieves chondrocyte inflammation by targeting miR-944/PGAP1 in osteoarthritis[J].Cell Cycle,2022,21(19):2038-2050.
[16] ZUO Y Z,XIONG C J,GAN X W,et al.LncRNA HAGLR silencing inhibits IL-1β-induced chondrocytes inflammatory injury via miR-130a-3p/JAK1 axis[J].J Orthop Surg Res,2023,18(1):203.
[17] GAN K F,WU W,LI J,et al.Positive feedback loop of lncRNA FAM201A/miR-146a-5p/POU2F1 regulates IL-1β-induced chondrocyte injury in vitro[J].Mol Med Rep,2022,25(1):20.
[18] 马鑫,朱涛.LINC00847促进乳腺癌细胞的增殖、迁移和侵袭[J].临床与实验病理学杂志,2022,38(1):15-20.
[19] HAO S X,YAO Z,LIU Y F.LINC00847 drives pancreatic cancer progression by targeting the miR-455-3p/HDAC4 axis[J].Arch Med Sci,2024,20(3):847-862.
[20] SUN W C,YUE J J,CUI Y X,et al.Wedelolactone alleviates inflammation and cartilage degeneration by suppressing the NF-κB signaling pathway in osteoarthritis[J].Int Immunopharmacol,2024,143(Pt 1):113359.
[21] 王孟宏.1.SHED外泌体miR-100-5p抑制mTOR缓解颞下颌关节骨关节炎 2.疼痛中心性量表在疼痛颞下颌关节紊乱病中的应用[D].重庆:重庆医科大学,2019.
[22] LI K L,YAN G H,HUANG H J,et al.Anti-inflammatory and immunomodulatory effects of the extracellular vesicles derived from human umbilical cord mesenchymal stem cells on osteoarthritis via M2 macrophages[J].J Nanobiotechno-logy,2022,20(1):38.
[23] LEWIS A,SÁNCHEZ S,BERTI G,et al.Small-molecule Wnt inhibitors are a potential novel therapy for intestinal fibrosis in Crohns disease[J].Clin Sci(Lond),2022,136(19):1405-1423.
[24] CHEN X C,MA T C,CHEN Y F,et al.USP14 promotes osteoarthritis progression by deubiquitinating FZD8 to activate the Wnt/β-catenin signaling pathway[J].Immunobiology,2025,230(3):152905.
[25] WANG Y Y,ZHENG X Y,LUO D X,et al.MiR-99a alleviates apoptosis and extracellular matrix degradation in experimentally induced spine osteoarthritis by targeting FZD8[J].BMC Musculoskelet Disord,2022,23(1):872.

相似文献/References:

[1]孟维娜,明立功,王新德,等.关节镜下清理联合腓骨近1/3段截骨治疗膝骨关节炎[J].中医正骨,2015,27(11):40.
[2]明立功,孟维娜,王新德,等.腓骨近端截骨治疗内侧间室膝骨关节炎的近期疗效观察[J].中医正骨,2015,27(10):25.
[3]张杰,王人彦,张玉柱.膝骨关节炎的治疗进展[J].中医正骨,2015,27(10):68.
[4]梁朝,蔡静怡,闫立,等.针刀疗法改善膝骨关节炎早期疼痛症状的疗效评价[J].中医正骨,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(03):9.
[5]王建武,党建军,李强,等.四联疗法治疗膝骨关节炎[J].中医正骨,2015,27(08):44.
[6]刘红娟,郭会利,郭树农.云克联合中药治疗膝骨关节炎的护理[J].中医正骨,2015,27(08):75.
[7]陈卫衡.探索建立系统的膝骨关节炎中医临床科研范式 和理论体系[J].中医正骨,2015,27(07):1.
[8]郑春松,叶蕻芝,李西海,等.透骨消痛胶囊中补肾柔肝药和活血祛风药治疗 骨关节炎作用方式的计算机模拟比较[J].中医正骨,2015,27(07):6.
　ZHENG Chunsong,YE Hongzhi,LI Xihai,et al.Comparison of the mode of action of Bushen Rougan(补肾柔肝)drugs versus Huoxue Qufeng(活血祛风)drugs contained in Tougu Xiaotong Jiaonang(透骨消痛胶囊)for the treatment of osteoarthritis:A computer simulation study[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2015,27(03):6.
[9]帅波,沈霖,杨艳萍,等.加味青娥丸治疗膝骨关节炎的作用机制研究[J].中医正骨,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(03):15.
[10]梅其杰,袁长深,段戡,等.壮药骨痹方烫熨联合运动疗法治疗膝骨关节炎的临床研究[J].中医正骨,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(03):27.
[11]郑春松,叶蕻芝,李西海,等.独活寄生汤含药血清对白细胞介素1β诱导的 退变关节软骨细胞中基质金属蛋白酶 和环氧化酶2表达的影响[J].中医正骨,2015,27(12):1.
　ZHENG Chunsong,YE Hongzhi,LI Xihai,et al.Impact of Duhuo Jisheng Tang(独活寄生汤)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(03):1.
[12]林木南,林艳红,刘献祥,等.温热疏密波对膝骨关节炎模型大鼠软骨细胞 RAS/丝裂原活化蛋白激酶信号通路的影响[J].中医正骨,2016,28(02):1.
　LIN Munan,LIN Yanhong,LIU Xianxiang,et al.Effect of warm sparse-dense wave on RAS/mitogen-activated protein kinase signaling pathway in chondrocytes of knee osteoarthritis rat models[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2016,28(03):1.
[13]原晓强,金王东,周云婧,等.纯化血小板对大鼠软骨细胞增殖及膝骨关节炎大鼠软骨修复的作用研究[J].中医正骨,2016,28(12):6.
　YUAN Xiaoqiang,JIN Wangdong,ZHOU Yunjing,et al.Effect of purified platelet rich plasma on chondrocyte proliferation in rats and cartilage repair in rats with knee osteoarthritis:an experimental study[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2016,28(03):6.
[14]刘启明,罗统富,董黎强,等.植物雌激素类中药延缓关节软骨细胞退变的研究进展[J].中医正骨,2017,29(05):27.
[15]叶锦霞,付长龙,林洁,等.透骨消痛胶囊对毒胡萝卜素诱导的内质网应激PEKR信号通路介导的大鼠体外培养关节软骨细胞凋亡的影响[J].中医正骨,2017,29(06):1.
　YE Jinxia,FU Changlong,LIN Jie,et al.Effect of Tougu Xiaotong Jiaonang(透骨消痛胶囊)on apoptosis mediated by endoplasmic reticulum stress(PEKR signaling pathway)and induced by thapsigargin in rat's articular chondrocytes cultured in vitro[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2017,29(03):1.
[16]何晓娟,林平冬,马玉环,等.独活寄生汤含药血清抑制白细胞介素1β诱导的软骨细胞炎症反应的作用机制研究[J].中医正骨,2017,29(08):1.
　HE Xiaojuan,LIN Pingdong,MA Yuhuan,et al.Study on mechanism of action of Duhuo Jisheng Tang(独活寄生汤)medicated serum in inhibiting inflammatory reaction induced by interleukin-1 beta in chondrocytes[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2017,29(03):1.
[17]郑文伟,何晓娟,贾良良,等.跳骨片含药血清抑制脂多糖诱导的软骨细胞炎症反应的作用机制研究[J].中医正骨,2017,29(08):8.
　ZHENG Wenwei,HE Xiaojuan,JIA Liangliang,et al.Study on mechanism of action of Tiaogu Pian(跳骨片)medicated serum in inhibiting inflammatory reaction induced by lipopolysaccharides in chondrocytes[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2017,29(03):8.
[18]陈世宣,刘益杰,胡笑燊,等.基于瞬时受体电位香草素亚家族4信号通路探讨牛蒡子苷元对体外培养软骨细胞增殖及Ⅱ型胶原蛋白和软骨蛋白聚糖表达的影响[J].中医正骨,2017,29(10):13.
　CHEN Shixuan,LIU Yijie,HU Xiaoshen,et al.An experimental study of effect of arctigenin on proliferation of chondrocyte cultured in vitro and expression of typeⅡcollagen protein and aggrecan based on the transient receptor potential vanilloid 4 signaling pathway[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2017,29(03):13.
[19]陈俊,吴广文,许惠凤,等.独活寄生汤含药血清对大鼠退变软骨细胞蛋白激酶 R样内质网激酶/免疫球蛋白结合蛋白信号通路的影响[J].中医正骨,2018,30(08):1.
　CHEN Jun,WU Guangwen,XU Huifeng,et al.Effect of Duhuo Jisheng Tang(独活寄生汤)medicated serum on protein kinase R-like endoplasmic reticulum kinase/immunoglobulin-binding protein signaling pathway in degenerated chondrocytes of rats[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2018,30(03):1.
[20]许丽梅,李慧,许云腾,等.基于NF-κB信号通路探讨独活寄生汤抑制脂多糖诱导的软骨细胞炎症反应的作用机制[J].中医正骨,2019,31(07):9.
　XU Limei,LI Hui,XU Yunteng,et al.An experimental study of mechanism of action of Duhuo Jisheng Tang(独活寄生汤)in inhibiting inflammatory reaction induced by lipopolysaccharide in chondrocytes based on NF-κB signaling pathway[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2019,31(03):9.

备注/Memo

备注/Memo:
基金项目:2022年佛山市自筹经费类科技创新项目(2220001003933)
通信作者:梁伟财 E-mail:lwc163613@163.com
(收稿日期:2025-06-18 本文编辑:吕宁)
更新日期/Last Update: 2026-03-20