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[1]張華燕,何援軍.薯蕷皂苷元改善類風(fēng)濕關(guān)節(jié)炎模型大鼠關(guān)節(jié)腫脹的效果及作用機(jī)制研究[J].中醫(yī)正骨,2021,33(04):44-50.
　ZHANG Huayan,HE Yuanjun.Efficacy and mechanism of diosgenin against joint swelling in rat models with rheumatoid arthritis[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2021,33(04):44-50.
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薯蕷皂苷元改善類風(fēng)濕關(guān)節(jié)炎模型大鼠關(guān)節(jié)腫脹的效果及作用機(jī)制研究()
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《中醫(yī)正骨》[ISSN:1001-6015/CN:41-1162/R]

卷:
第33卷
期數(shù):
2021年04期
頁碼:
44-50
欄目:
基礎(chǔ)研究
出版日期:
2021-04-20

文章信息/Info

Title:
Efficacy and mechanism of diosgenin against joint swelling in rat models with rheumatoid arthritis
作者:
張華燕; 何援軍
(浙江衢化醫(yī)院,浙江 衢州 324004)
Author(s):
ZHANG Huayan; HE Yuanjun
Zhejiang Quhua Hospital,Quzhou 324004,Zhejiang,China
關(guān)鍵詞:
關(guān)節(jié)炎; 類風(fēng)濕;  薯蕷皂苷元;  Nod樣受體蛋白3炎性體;  動(dòng)物實(shí)驗(yàn);  大鼠; Sprague-Dawley
Keywords:
arthritis; rheumatoid;  diosgenin;  Nod-like receptor protein 3 inflammasome;  animal experimentation;  rats;  Sprague-Dawley
摘要:
目的:探討薯蕷皂苷元改善類風(fēng)濕關(guān)節(jié)炎(rheumatoid arthritis,RA)模型大鼠關(guān)節(jié)腫脹的效果及可能的作用機(jī)制。方法:從70只6周齡SPF級(jí)雄性SD大鼠中隨機(jī)選取55只,建立Ⅱ型膠原誘導(dǎo)的RA大鼠模型,剩余15只納入空白組。將造模成功的48只大鼠隨機(jī)分為模型組、激活劑組和薯蕷皂苷元組,每組各16只。薯蕷皂苷元組以薯蕷皂苷元干預(yù),激活劑組以尼日利亞菌素鈉鹽干預(yù),空白組、模型組僅給予生理鹽水。每天干預(yù)1次,共干預(yù)2周。干預(yù)結(jié)束后,采用關(guān)節(jié)炎指數(shù)評(píng)定各組大鼠的關(guān)節(jié)腫脹情況,檢測外周血炎癥因子[白細(xì)胞介素(interleukin,IL)-1β、IL-6、腫瘤壞死因子(tumor necrosis factor-α,TNF-α)]和氧化應(yīng)激因子[丙二醛(malondialdehyde,MDA)、超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽(glutathione,GSH)]含量,取大鼠關(guān)節(jié)滑膜組織HE染色后進(jìn)行病理學(xué)觀察,并測定大鼠滑膜組織中Nod樣受體蛋白3(Nod-like receptor protein 3,NLRP3)炎性體信號(hào)通路相關(guān)蛋白[IL-1β、半胱氨酸天冬氨酸蛋白酶1(Caspase-1)及NLRP3]含量。結(jié)果:①關(guān)節(jié)腫脹情況。模型組、激活劑組及薯蕷皂苷元組大鼠的關(guān)節(jié)炎指數(shù)比較,差異有統(tǒng)計(jì)學(xué)意義[(3.43±0.32)分,(2.44±0.20)分,(0.86±0.10)分,F=14.974,P=0.000]。激活劑組和薯蕷皂苷元組的關(guān)節(jié)炎指數(shù)均低于模型組(P=0.001,P=0.000),薯蕷皂苷元組的關(guān)節(jié)炎指數(shù)低于激活劑組(P=0.000)。②外周血炎癥因子含量。空白組、模型組、激活劑組及薯蕷皂苷元組大鼠的血清IL-1β、IL-6、TNF-α含量比較,組間差異均有統(tǒng)計(jì)學(xué)意義[IL-1β:(128.82±13.71)μg·mL-1,(279.44±28.21)μg·mL-1,(213.12±20.65)μg·mL-1,(176.76±19.25)μg·mL-1,F=36.554,P=0.000; IL-6:(119.56±12.42)μg·mL-1,(271.18±27.11)μg·mL-1,(198.43±21.36)μg·mL-1,(146.85±15.72)μg·mL-1,F=28.643,P=0.000; TNF-α:(203.63±22.08)μg·mL-1,(328.91±36.22)μg·mL-1,(275.88±27.52)μg·mL-1,(237.89±23.12)μg·mL-1,F=41.832,P=0.000]。模型組、激活劑組及薯蕷皂苷元組的血清IL-1β、IL-6、TNF-α含量均高于空白組(IL-1β:P=0.001,P=0.000,P=0.002; IL-6:P=0.001,P=0.000,P=0.016; TNF-α:P=0.000,P=0.002,P=0.043); 激活劑組和薯蕷皂苷元組的血清IL-1β、IL-6、TNF-α含量均低于模型組(IL-1β:P=0.003,P=0.000; IL-6:P=0.002,P=0.000; TNF-α:P=0.031,P=0.001); 薯蕷皂苷元組的血清IL-1β、IL-6、TNF-α含量均低于激活劑組(P=0.021,P=0.002,P=0.046)。③外周血氧化應(yīng)激因子含量。空白組、模型組、激活劑組及薯蕷皂苷元組大鼠的血漿MDA、SOD、GSH含量比較,組間差異均有統(tǒng)計(jì)學(xué)意義[MDA:(10.24±1.87)μmol·L-1,(36.51±3.63)μmol·L-1,(21.33±2.42)μmol·L-1,(16.37±1.85)μmol·L-1,F=15.632,P=0.000; SOD:(145.52±14.72)U·mL-1,(40.41±6.96)U·mL-1,(79.42±8.32)U·mL-1,(106.12±10.22)U·mL-1,F=21.334,P=0.000; GSH:(38.54±3.82)U·mL-1,(14.77±2.12)U·mL-1,(21.63±2.19)U·mL-1,(28.63±2.97)U·mL-1,F=13.213,P=0.000]。模型組、激活劑組及薯蕷皂苷元組的血漿MDA含量均高于空白組(P=0.000,P=0.000,P=0.001),血漿SOD、GSH含量均低于空白組(SOD:P=0.000,P=0.000,P=0.001; GSH:P=0.000,P=0.000,P=0.002); 激活劑組及薯蕷皂苷元組的血漿MDA含量均低于模型組(P=0.000,P=0.000),血漿SOD、GSH含量均高于模型組(SOD:P=0.000,P=0.000; GSH:P=0.001,P=0.000); 激活劑組的血漿MDA含量高于薯蕷皂苷元組(P=0.007),血漿SOD、GSH含量均低于薯蕷皂苷元組(P=0.002,P=0.003)。④滑膜組織病理學(xué)觀察結(jié)果。空白組關(guān)節(jié)滑膜組織結(jié)構(gòu)、形態(tài)正常; 模型組關(guān)節(jié)滑膜組織有炎性細(xì)胞浸潤,滑膜細(xì)胞增生,血管擴(kuò)張,形成血栓; 激活劑組關(guān)節(jié)滑膜組織病理變化較模型組改善,但有輕微滑膜細(xì)胞增生; 薯蕷皂苷元組關(guān)節(jié)滑膜組織病理變化明顯改善。⑤滑膜組織NLRP3炎性體信號(hào)通路相關(guān)蛋白含量。空白組、模型組、激活劑組及薯蕷皂苷元組大鼠關(guān)節(jié)滑膜組織IL-1β、Caspase-1、NLRP3含量比較,組間差異均有統(tǒng)計(jì)學(xué)意義(IL-1β:0.46±0.07,1.02±0.10,0.72±0.08,0.56±0.06,F=31.025,P=0.000; Caspase-1:0.54±0.08,1.16±0.12,0.90±0.10,0.73±0.08,F=23.658,P=0.000; NLRP3:0.69±0.08,1.27±0.12,1.01±0.11,0.88±0.09,F=28.754,P=0.000); 模型組、激活劑組及薯蕷皂苷元組滑膜組織IL-1β、Caspase-1、NLRP3含量均高于空白組(IL-1β:P=0.000,P=0.001,P=0.042; Caspase-1:P=0.000,P=0.000,P=0.006; -----------------------------------------------
Abstract:
To explore the efficacy of diosgenin against joint swelling in rat models with rheumatoid arthritis(RA)and its possible mechanism.Methods:From the 70 6-week-old SPF-grade male Sprague-Dawley(SD)rats,55 rats were randomly selected and intracutaneously injected with typeⅡcollagen for inducing RA,and the remaining 15 rats were classified into blank group.The successfully modeled 48 rats were then randomly assigned to model group,activator group and diosgenin group,16 rats in each group.The rats in diosgenin group were treated with diosgenin,the ones in activator group with nigericin sodium salt,and the ones in blank group and model group with normal saline(NS),once a day for consecutive two weeks.After the end of intervention,the joint swelling of rats in each group was evaluated based on the arthritis index(AI).The levels of inflammatory cytokines including interleukin(IL)-1β,IL-6 and tumor necrosis factor-α(TNF-α)and oxidative stress(OS)inducers including malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione(GSH)in peripheral blood were detected.The synovial tissues of rat joints were stained with hematoxylin-eosin(HE)for pathological observation,followed by the determination of the expression levels of related proteins including IL-1β,cysteinyl aspartate-specific protease-1(Caspase-1)and Nod-like receptor protein 3(NLRP3)in the NLRP3 inflammasome signaling pathway.Results:The difference in AI scores among model group,activator group and diosgenin group was statistically significant(3.43±0.32,2.44±0.20,0.86±0.10 points,F=14.974,P=0.000).The AI scores of activator group and diosgenin group were lower than that of model group(P=0.001,P=0.000),and that in diosgenin group was even lower(P=0.000).The comparison of serum IL-1β,IL-6 and TNF-α levels of rats among blank group,model group,activator group and diosgenin group revealed significant differences(IL-1β:128.82±13.71,279.44±28.21,213.12±20.65,176.76±19.25 μg/mL,F=36.554,P=0.000; IL-6:119.56±12.42,271.18±27.11,198.43±21.36,146.85±15.72 μg/mL,F=28.643,P=0.000; TNF-α:203.63±22.08,328.91±36.22,275.88±27.52,237.89±23.12 μg/mL,F=41.832, P=0.000).The serum IL-1β,IL-6 and TNF-α levels in model group,activator group and diosgenin group were all higher than those in blank group(IL-1β:P=0.001,P=0.000,P=0.002; IL-6:P=0.001,P=0.000,P=0.016; TNF-α:P=0.000,P=0.002,P=0.043)...

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備注/Memo

備注/Memo:
基金項(xiàng)目:2018年度衢州市科技計(jì)劃指導(dǎo)性項(xiàng)目(第二批)(2018127)
通訊作者:張華燕 E-mail:[email protected]
更新日期/Last Update: 1900-01-01