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[1]伏厚宇,揭立士,茆軍,等.膝痹寧Ⅱ干預小鼠膝骨關節(jié)炎寒濕痹阻證的效果及作用機制研究[J].中醫(yī)正骨,2025,37(04):20-29.
　FU Houyu,JIE Lishi,MAO Jun,et al.Efficacy and mechanism of Xibi NingⅡ(膝痹寧Ⅱ)against knee osteoarthritis with cold-dampness stagnation syndrome in mice:an experimental study[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2025,37(04):20-29.
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膝痹寧Ⅱ干預小鼠膝骨關節(jié)炎寒濕痹阻證的效果及作用機制研究()
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《中醫(yī)正骨》[ISSN:1001-6015/CN:41-1162/R]

卷:
第37卷
期數:
2025年04期
頁碼:
20-29
欄目:
基礎研究
出版日期:
2025-04-20

文章信息/Info

Title:
Efficacy and mechanism of Xibi NingⅡ(膝痹寧Ⅱ)against knee osteoarthritis with cold-dampness stagnation syndrome in mice:an experimental study
作者:
伏厚宇; 揭立士; 茆軍; 張農山; 黃正泉; 丁亮; 邢潤麟; 梅偉; 殷松江; 吳鵬; 李曉辰; 馬振源; 王培民; 張立
南京中醫(yī)藥大學附屬醫(yī)院,江蘇 南京 210029
Author(s):
FU Houyu; JIE Lishi; MAO Jun; ZHANG Nongshan; HUANG Zhengquan; DING Liang; XING Runlin; MEI Wei; YIN Songjiang; WU Peng; LI Xiaochen; MA Zhenyuan; WANG Peimin; ZHANG Li
Affiliated Hospital of Nanjing University of Chinese Medicine,Nanjing 210029,Jiangsu,China
關鍵詞:
骨關節(jié)炎; 膝;  寒濕;  痹證;  膝痹寧Ⅱ;  疼痛;  敏化;  神經節(jié); 脊;  滑膜;  腫瘤壞死因子;  白細胞介素類;  瞬時受體電位通道;  降鈣素基因相關肽;  神經生長因子;  小鼠
Keywords:
osteoarthritis; knee;  cold dampness;  arthromyodynia;  Xibi Ning Ⅱ;  pain;  sensitization;  ganglia; spinal;  synovial membrane;  tumor necrosis factors;  interleukins;  transient receptor potential channels;  calcitonin gene-related peptide;  nerve growth factor;  mice
摘要:
目的:探討膝痹寧Ⅱ干預小鼠膝骨關節(jié)炎(knee osteoarthritis,KOA)寒濕痹阻證的效果及作用機制。方法:將40只C57BL/6J小鼠隨機分為假手術組、模型組、膝痹寧Ⅱ組、蠲痹湯組,每組10只。模型組、膝痹寧Ⅱ組、蠲痹湯組小鼠均行半月板失穩(wěn)術,并在術后將小鼠置于人工氣候箱(濕度60%、溫度4 ℃、風速6 m·s-1)中構建KOA寒濕痹阻證模型; 假手術組僅切開膝關節(jié)處皮膚。造模成功后,膝痹寧Ⅱ組和蠲痹湯組小鼠分別用0.26 mL的膝痹寧Ⅱ藥液(生藥濃度1.0 g·mL-1)和0.26 mL的蠲痹湯藥液(生藥濃度1.9 g·mL-1)灌胃,假手術組和模型組小鼠均給予等量蒸餾水灌胃。每日給藥1次,連續(xù)給藥28 d。分別于造模開始前、造模結束后第7天及藥物干預7 d、14 d、21 d、28 d,測定各組小鼠冷刺激縮足閾值和機械刺激縮足閾值。藥物干預28 d后,采用ELISA法檢測小鼠血清中腫瘤壞死因子(tumor necrosis factor,TNF)-α、白細胞介素(interleukin,IL)-1β和IL-6的含量,分別采用HE染色、Masson染色、天狼星紅染色觀察小鼠膝關節(jié)滑膜組織病理變化,采用免疫熒光法檢測小鼠L3～L5背根神經節(jié)(dorsal root ganglia,DRG)組織中瞬時受體電位錨蛋白1(transient receptor potential ankyrin 1,TRPA1)、瞬時受體電位香草酸1(transient receptor potential vanilloid 1,TRPV1)、瞬時受體電位褪黑素8(transient receptor potential melastatin 8,TRPM8)通道,采用Western Bolt法檢測L3～L5DRG組織中TRPA1、TRPV1、TRPM8、降鈣素基因相關肽(calcitonin gene related peptide,CGRP)、神經生長因子(nerve growth factor,NGF)的蛋白表達水平。結果:①小鼠冷刺激縮足閾值和機械刺激縮足閾值測定結果。造模結束后第7天,模型組、膝痹寧Ⅱ組、蠲痹湯組小鼠冷刺激縮足閾值、機械刺激縮足閾值均低于假手術組(P=0.000,P=0.000,P=0.000; P=0.000,P=0.000,P=0.000),膝痹寧Ⅱ組、蠲痹湯組小鼠冷刺激縮足閾值、機械刺激縮足閾值與模型組的差異均無統(tǒng)計學意義(P=0.782,P=0.957; P=0.988,P=0.986),膝痹寧Ⅱ組小鼠冷刺激縮足閾值、機械刺激縮足閾值與蠲痹湯組的差異均無統(tǒng)計學意義(P=0.990,P=0.915); 藥物干預7 d、14 d、21 d、28 d,模型組小鼠冷刺激縮足閾值、機械刺激縮足閾值均低于假手術組、膝痹寧Ⅱ組、蠲痹湯組(干預7 d:P=0.000,P=0.000,P=0.000; P=0.000,P=0.000,P=0.000。干預14 d:P=0.000,P=0.005,P=0.000; P=0.000,P=0.000,P=0.000。干預21 d:P=0.000,P=0.000,P=0.000; P=0.000,P=0.000,P=0.000。干預 28 d:P=0.000,P=0.000,P=0.000; P=0.000,P=0.000,P=0.000),膝痹寧Ⅱ組小鼠冷刺激縮足閾值、機械刺激縮足閾值與蠲痹湯組的差異均無統(tǒng)計學意義(干預7 d:P=0.714,P=0.767; 干預14 d:P=0.781,P=0.997; 干預21 d:P=0.994,P=0.762; 干預28 d:P=0.892,P=0.961)。②小鼠血清中TNF-α、IL-6、IL-1β含量測定結果。模型組小鼠血清中TNF-α、IL-6、IL-1β含量均高于假手術組、膝痹寧Ⅱ組、蠲痹湯組(TNF-α:P=0.000,P=0.000,P=0.000; IL-6:P=0.000,P=0.000,P=0.000; IL-1β:P=0.000,P=0.000,P=0.000),膝痹寧Ⅱ組小鼠血清中TNF-α、IL-6、IL-1β含量與蠲痹湯組的差異均無統(tǒng)計學意義(P=0.996,P=0.950,P=0.799)。③小鼠膝關節(jié)滑膜組織病理學觀察結果。HE染色顯示,模型組滑膜細胞排列紊亂,炎性浸潤明顯; 膝痹寧Ⅱ組、蠲痹湯組滑膜細胞排列較整齊,滑膜結構趨于正常,炎性浸潤明顯減少。Masson染色顯示,模型組滑膜膠原纖維排列紊亂,膠原纖維沉積增多; 膝痹寧Ⅱ組、蠲痹湯組滑膜膠原纖維排列整齊,滑膜結構趨于正常,膠原纖維沉積明顯減少。天狼星紅染色顯示,模型組Ⅱ型膠原減少,膠原纖維排列紊亂; 膝痹寧Ⅱ組、蠲痹湯組Ⅱ型膠原增多,膠原纖維排列較整齊。④小鼠L3～L5DRG組織中TRPA1、TRPV1、TRPM8通道檢測結果。免疫熒光染色顯示,假手術組TRPA1、TRPV1、TRPM8熒光強度最弱,模型組熒光強度最強,膝痹寧Ⅱ和蠲痹湯組熒光強度較模型組減弱。⑤小鼠L3～L5DRG組織中TRPA1、TRPM8、TRPV1、NGF、CGRP的蛋白表達水平檢測結果。模型組小鼠L3～L5DRG組織中TRPA1、TRPM8、TRPV1、NGF、CGRP的蛋白相對表達量均高于假手術組、膝痹寧Ⅱ組、蠲痹湯組(TRPA1:P=0.000,P=0.000,P=0.000; TRPM8:P=0.000,P=0.000,P=0.000; TRPV1:P=0.000,P=0.000,P=0.000; NGF:P=0.000,P=0.000,P=0.000; CGRP:P=0.000,P=0.000,P=0.000),膝痹寧Ⅱ組TRPA1、TRPM8、TRPV1、NGF、CGRP的蛋白相對表達量與蠲痹湯組的差異均無統(tǒng)計學意義(P=0.939,P=0.998,P=0.981,P=0.961,P=0.794)。結論:膝痹寧Ⅱ能夠減輕KOA寒濕痹阻證模型小鼠痛覺敏化和滑膜炎癥,療效與蠲痹湯相當,其作用機制可能與其能抑制DRG組織中TRP通道激活有關。
Abstract:
Objective:To observe the outcomes of Xibi NingⅡ(膝痹寧Ⅱ,XBNⅡ)against knee osteoarthritis(KOA)with the syndrome of cold-dampness stagnation in mice,and to explore its underlying mechanism.Methods:Forty C57BL/6J mice were selected and randomized into sham-operated group,model group,XBNⅡgroup and Juanbi Tang(蠲痹湯,JBT)group,with 10 ones in each group.All mice but the ones in sham-operated group were subjected to destabilization of the medial meniscus(DMM)surgery for inducing KOA,and then housed in an artificial climate chamber(humidity:60%,temperature:4 ℃,wind speed:6 m/s)for further inducing the syndrome of cold-dampness stagnation,while the ones in sham-operated group were merely incised the skin at the corresponding site.After successful modeling,the mice in XBNⅡgroup and JBT group were intervened by intragastric administration with 0.26 mL XBNⅡsolution(the crude drug concentration was 1.0 g/mL)and 0.26 mL JBT solution(the crude drug concentration was 1.9 g/mL),respectively,while the ones in the sham-operated group and model group with the same dose of distilled water,once a day for consecutive 28 days.The cold and mechanical stimulation paw withdrawal thresholds(PWTs)were measured before the modeling,on day 7 after the end of the modeling and after 7-,14-,21- and 28-day drug intervention,respectively.After 28-day drug intervention,the serum levels of tumor necrosis factor(TNF)-α,interleukin(IL)-1β,and IL-6 were detected by ELISA.After that,the mice knee synovial tissues were harvested and stained with HE staining,Masson staining,and Sirius red staining,respectively,to observe the pathological changes.Furthermore,the channels of transient receptor potential ankyrin 1(TRPA1),transient receptor potential vanilloid 1(TRPV1),and transient receptor potential melastatin 8(TRPM8)in the L3-L5 dorsal root ganglia(DRG)tissues was detected using immunofluorescence,and the protein expression levels of TRPA1,TRPV1,TRPM8,calcitonin gene related peptide(CGRP)and nerve growth factor(NGF)in the L3-L5 DRG tissues were detected using Western Blot.Results:①The cold and mechanical stimulation PWTs.On day 7 after the end of the modeling,the cold and mechanical stimulation PWTs were lower in model group,XBNⅡgroup and JBT group compared to sham-operated group(P=0.000,P=0.000,P=0.000; P=0.000,P=0.000,P=0.000),with no significant differences between XBNⅡgroup and model group,between JBT group and model group,between XBNⅡgroup and JBT group(P=0.782,P=0.957; P=0.988,P=0.986; P=0.990,P=0.915).After 7-,14-,21- and 28-day drug intervention,the cold and mechanical stimulation PWTs were lower in model group compared to sham-operated group,XBNⅡgroup and JBT group(7-day intervention:P=0.000,P=0.000,P=0.000; P=0.000,P=0.000,P=0.000.14-day intervention:P=0.000,P=0.005,P=0.000; P=0.000,P=0.000,P=0.000.21-day intervention:P=0.000,P=0.000,P=0.000; P=0.000,P=0.000,P=0.000.28-day intervention:P=0.000,P=0.000,P=0.000; P=0.000,P=0.000,P=0.000),with no significant differences between XBNⅡgroup and JBT group(7-day intervention:P=0.714,P=0.767; 14-day intervention:P=0.781,P=0.997; 21-day intervention:P=0.994,P=0.762; 28-day intervention:P=0.892,P=0.961).②The serum levels of TNF-α,IL-6,and IL-1β.The serum levels of TNF-α,IL-6,and IL-1β were higher in model group compared to sham-operated group,XBNⅡgroup and JBT group(TNF-α:P=0.000,P=0.000,P=0.000; IL-6:P=0.000,P=0.000,P=0.000; IL-1β:P=0.000,P=0.000,P=0.000),with no significant differences between XBNⅡgroup and JBT group(P=0.996,P=0.950,P=0.799).③The pathological changes in the knee synovial tissues.HE staining showed that,the changes,manifesting as disorderedly arranged synovial cells with obviously inflammatory infiltration,were observed in the knee synovial tissues of mice in model group; while,compared with that of model group,the knee synovial tissues in mice of XBNⅡgroup and JBT group was significantly improved,manifesting as neatly arranged synovial cells,with basically normalized synovial tissue architecture,and markedly reduced inflammatory infiltration.Masson staining revealed that,in model group,the synovial collagen fibers were disorderedly arranged with increased collagen fiber deposition; while,which was improved in XBNⅡgroup and JBT group,manifesting as aligned synovial collagen fibers with basically normalized synovial tissue architecture and significantly decreased collagen fiber deposition.Sirius red staining showed that,reduced typeⅡcollagen and disorganized collagen fiber arrangement were observed in the knee synovial tissues of mice in model group,while,compared with that of model group,the knee synovial tissues in mice of XBNⅡgroup and JBT group exhibited increased typeⅡcollagen with more improved arrangement in collagen fiber organization.④The channels of TRPA1,TRPV1 and TRPM8 in the L3-L5 DRG tissues.The immunofluorescence staining showed that the weakest fluorescence intensity of TRPA1,TRPV1 and TRPM8 was observed in sham-operated group,the strongest in model group,and attenuated in XBNⅡgroup and JBT group compared to model group.⑤The protein expression levels of TRPA1,TRPM8,TRPV1,NGF,and CGRP in the L3-L5 DRG tissues.The relative protein expression levels of TRPA1,TRPM8,TRPV1,NGF,and CGRP in the L3-L5 DRG tissues were higher in model group compared to sham-operated group,XBNⅡgroup and JBT group(TRPA1:P=0.000,P=0.000,P=0.000; TRPM8:P=0.000,P=0.000,P=0.000; TRPV1:P=0.000,P=0.000,P=0.000; NGF:P=0.000,P=0.000,P=0.000; CGRP:P=0.000,P=0.000,P=0.000),with no significant differences between XBNⅡgroup and JBT group(P=0.939,P=0.998,P=0.981,P=0.961,P=0.794).Conclusion:XBNⅡcan alleviate pain hypersensitivity and synovial inflammation in KOA model mice with the syndrome of cold-dampness stagnation,and it is similar to JBT in clinical efficacy.It may work by inhibiting the activation of TRP channels in DRG tissues.

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備注/Memo

備注/Memo:
基金項目:國家自然科學基金項目(82305276); 江蘇省醫(yī)學重點學科和醫(yī)學重點實驗室項目(JSDW202252); 江蘇省中醫(yī)院臨床醫(yī)學創(chuàng)新中心發(fā)展規(guī)劃項目(Y2023zx05)
通訊作者:張立 E-mail:[email protected]
更新日期/Last Update: 1900-01-01