痛风药食两用2号方对痛风性关节炎寒证大鼠血清药效学影响的研究
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摘要
目的:研究痛风药食两用2号方对痛风性关节炎(Gouty arthritis,GA)寒证大鼠血清中αN已酰氨基葡糖苷酶(αNacetylglucosaminidase,αNAG)、β-半乳糖苷酶(β-galactosidase,β-gal)、超氧化物歧化酶(Superoxide dismutase,SOD)、尿酸(Uric acid,UA)、肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)的影响。方法:将32只SD大鼠随机分为正常组、模型组、阳性药组及寒证组,每组8只。除正常组外,其余各组大鼠在第7天于右足踝关节内注射尿酸钠溶液造模。寒证组大鼠每天置于低温环境(0±2)℃1 h,持续半个月,制造寒证证候模型。造模后阳性药组按1.5 mg/(kg·d)的剂量灌胃秋水仙碱;正常组和模型组灌胃等体积生理盐水,寒证组按22 g/kg的剂量灌胃痛风药食两用2号方,每天2次,连续给药7天。不同时间测量各组大鼠右后足踝关节的周长值,第15天用酶联免疫法测定血清中αNAG、β-gal、SOD、UA和TNF-α含量。结果:与正常组比较,模型组大鼠关节明显肿胀,血清中αNAG、β-gal、UA、TNF-α含量升高(P <0.01),提示造模成功。与模型组比较,寒证组大鼠关节肿胀程度显著改善(P <0.01);血清中αNAG、β-gal、UA、TNF-α含量显著降低(P <0.01)。结论:痛风药食两用2号方对GA寒证大鼠有治疗作用,其机制可能与抑制αNAG、β-gal、UA、TNF-α水平有关。
Objective:To study the effect of medicinal and edible No.2 prescription for gout on αN-acetylglucosaminidase(αNAG), β-galactosidase(β-gal), superoxide dismutase(SOD), uric acid(UA) and tumor necrosis factor-α(TNF-α) in serum in rats with gouty arthritis(GA) with cold syndrome. Methods: A total of 32 SD rats were randomly divided into the normal group, the model group, the positive medicine group and the cold syndrome group. Except those in the normal group,rats in other groups were injected sodium urate solution into the right ankle joint on the 7 th day for modeling. The rats in the cold syndrome group were exposed to low-temperature environment(0±2) °C for one hour every day for half a month to established the models with cold syndrome. After modeling, the positive medicine group was given 1.5 mg/(kg·d) of colchicine by gavage; the normal group and the model group were given saline of the same volume,and the cold syndrome group was given 22 g/kg of medicinal and edible No.2 prescription for gout by gavage. All groups were administrated twice a day for seven days. The perimeters of right ankle joint of rats in each group were measured at different time;the contents ofαNAG,β-gal,SOD,UA and TNF-α in serum were measured by enzyme-linked immunosorbent assay on the 15 th day.Results:Compared with those in the normal group,the joints of rats in the model group were obviously swollen,and the contents of αNAG,β-gal,UA and TNF-α in serum in the model group were increased(P < 0.01), suggesting that the modeling was successful. Compared with that in the model group,the degree of joint swelling in the cold syndrome group was significantly decreased(P < 0.01);the contents of αNAG,β-gal,UA and TNF-α in serum were significantly decreased(P < 0.01). Conclusion: Medicinal and edible No.2 prescription for gout has therapeutic effect in treating rats with gouty arthritis with cold syndrome,whose mechanism is probably related to the inhibition of the levels of αNAG,β-gal,UA and TNF-α.
Objective:To study the effect of medicinal and edible No.2 prescription for gout on αN-acetylglucosaminidase(αNAG), β-galactosidase(β-gal), superoxide dismutase(SOD), uric acid(UA) and tumor necrosis factor-α(TNF-α) in serum in rats with gouty arthritis(GA) with cold syndrome. Methods: A total of 32 SD rats were randomly divided into the normal group, the model group, the positive medicine group and the cold syndrome group. Except those in the normal group,rats in other groups were injected sodium urate solution into the right ankle joint on the 7 th day for modeling. The rats in the cold syndrome group were exposed to low-temperature environment(0±2) °C for one hour every day for half a month to established the models with cold syndrome. After modeling, the positive medicine group was given 1.5 mg/(kg·d) of colchicine by gavage; the normal group and the model group were given saline of the same volume,and the cold syndrome group was given 22 g/kg of medicinal and edible No.2 prescription for gout by gavage. All groups were administrated twice a day for seven days. The perimeters of right ankle joint of rats in each group were measured at different time;the contents ofαNAG,β-gal,SOD,UA and TNF-α in serum were measured by enzyme-linked immunosorbent assay on the 15 th day.Results:Compared with those in the normal group,the joints of rats in the model group were obviously swollen,and the contents of αNAG,β-gal,UA and TNF-α in serum in the model group were increased(P < 0.01), suggesting that the modeling was successful. Compared with that in the model group,the degree of joint swelling in the cold syndrome group was significantly decreased(P < 0.01);the contents of αNAG,β-gal,UA and TNF-α in serum were significantly decreased(P < 0.01). Conclusion: Medicinal and edible No.2 prescription for gout has therapeutic effect in treating rats with gouty arthritis with cold syndrome,whose mechanism is probably related to the inhibition of the levels of αNAG,β-gal,UA and TNF-α.
引文
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[15]刘磊,刘健,冯云霞,等.强直性脊柱炎患者血清超氧化物歧化酶的变化及相关因素分析[J].中国临床保健杂志,2012,15(5):478-481.
[16]姜德友,曲晓雪,陈飞,等.补肾利湿法对痛风性关节炎大鼠超氧化物歧化酶表达的影响[J].湖北中医药大学学报,2016,18(1):11-14.
[17]任丽,欧水平,陈灵,等.虎杖提取物及其有效部位的大鼠抗痛风性关节炎试验[J].中国实验方剂学杂志,2016,22(19):111-115.
[18]LEE H P,LIN Y Y,DUH C Y,et al.Lemnalol attenuates mastcell activation and osteoclast activity in a gouty arthritis model[J].Pharrn Pharrnacol,2015,67(2):274-285.
[19]吴晓蓉,张开凯,杨雷,等.原发性痛风肾功能损害影响因素分析[J].江苏医药,2015,41(24):3039-3040.
[20]OSHIMA J,CAMPISI J.Mammary cell proliferation and morphogenesis.Fundamentals of cell proliferation:control of the cell cycle[J].J Dairy Sci,1991,74:277-278.
[2]尹磊,林丽雅,李学峰.急性痛风性关节炎中西医治疗研究进展[J].河北医药,2017,39(5):751-756,759.
[3]张瑞芬,赵晶.痛风的药物治疗现状及展望[J].解放军药学学报,2007,23(6):438-441.
[4]高雪珍.痛风的治疗现状及预防原则[J].临床合理用药杂志,2009,2(8):94-96.
[5]杨雪芳,王永昌,王苗慧,等.痛风的发病机制与药物治疗研究进展[J].中医药导报,2014,20(6):89-92.
[6]CODERRE T J,WALL P D.Ankle joint urate arthritis in rat:provided useful tool for the evaluation of analysis and anti-arthritic anents[J].Pharm Biochem Behav,1988,29(3):461.
[7]成秀梅,杜惠兰,李丹.寒凝血瘀证动物模型的创建[J].中国中医基础医学杂志,2005,11(8):604-605.
[8]万春平,李兆福,徐翔峰,等.急性痛风性关节炎免疫学发病机制研究进展[J].风湿病与关节炎,2012,1(4):52-55.
[9]陈睿,赵萌,朱利利.中药泄浊除痹汤治疗痛风性关节炎疗效及安全性分析和抗炎作用机制[J].世界中医药,2017,12(9):2101-2104,2108.
[10]汤剑斌,丁琦.中药外敷治疗老年急性痛风性关节炎疗效观察[J].河北中医,2014,36(2):194-195.
[11]张征,朱宁,刘明琛,等.降浊定痛方联合秋水仙碱治疗痛风急性发作期的临床研究[J].中药药理与临床,2017,33(2):212-215.
[12]王笑青,张依山,时红磊.自拟痛风方治疗急性痛风性关节炎疗效观察[J].风湿病与关节炎,2017,6(8):48-50.
[13]吴蕊,王镁.痛风的中医治疗现状[J].山西医药杂志,2015,44(6):662-664.
[14]李共信.泄浊化瘀调益脾肾法治疗痛风112例[J].中医临床研究,2014,6(10):109-110.
[15]刘磊,刘健,冯云霞,等.强直性脊柱炎患者血清超氧化物歧化酶的变化及相关因素分析[J].中国临床保健杂志,2012,15(5):478-481.
[16]姜德友,曲晓雪,陈飞,等.补肾利湿法对痛风性关节炎大鼠超氧化物歧化酶表达的影响[J].湖北中医药大学学报,2016,18(1):11-14.
[17]任丽,欧水平,陈灵,等.虎杖提取物及其有效部位的大鼠抗痛风性关节炎试验[J].中国实验方剂学杂志,2016,22(19):111-115.
[18]LEE H P,LIN Y Y,DUH C Y,et al.Lemnalol attenuates mastcell activation and osteoclast activity in a gouty arthritis model[J].Pharrn Pharrnacol,2015,67(2):274-285.
[19]吴晓蓉,张开凯,杨雷,等.原发性痛风肾功能损害影响因素分析[J].江苏医药,2015,41(24):3039-3040.
[20]OSHIMA J,CAMPISI J.Mammary cell proliferation and morphogenesis.Fundamentals of cell proliferation:control of the cell cycle[J].J Dairy Sci,1991,74:277-278.
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