承德医学院学报
承德醫學院學報
승덕의학원학보
JOURNAL OF CHENGDE MEDICAL
2014年
1期
8-10
,共3页
杨会杰%阎昊%佟继铭%刘永平
楊會傑%閻昊%佟繼銘%劉永平
양회걸%염호%동계명%류영평
赤雹根总皂苷%佐剂性关节炎%TNF-α%IL-1β%IL-6
赤雹根總皂苷%佐劑性關節炎%TNF-α%IL-1β%IL-6
적박근총조감%좌제성관절염%TNF-α%IL-1β%IL-6
Total saponins of Thladiantha dubia root (TSTDR)%Adjuvant arthritis%TNF-α%IL-1β%IL-6
目的：观察赤雹根总皂苷(TSTDR)对佐剂性关节炎(AA)大鼠脾脏指数和脾脏肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)表达的影响。方法：雄性SD大鼠60只随机分为正常对照组，模型组，TSTDR低(40mg/kg/d)、中(80mg/kg/d)、高(160mg/kg/d)剂量组和雷公藤多苷组(12mg/kg/d)。大鼠右后足跖部皮下注射弗氏完全佐剂0.1ml建立AA大鼠模型，成模后各用药组大鼠分别灌胃给予相应药物21d。计算大鼠的脾脏指数，免疫组织化学染色法检测各组大鼠脾脏TNF-α、IL-1β、IL-6的表达。结果：TSTDR中、高剂量组大鼠的脾脏指数显著低于模型组(P＜0.01，P＜0.05)。TSTDR各剂量组大鼠脾脏TNF-α、IL-1β、IL-6的表达水平明显低于模型组(P＜0.01，P＜0.05)；并且，TSTDR中剂量组、TSTDR高剂量组大鼠脾脏TNF-α、IL-1β、IL-6的表达水平明显低于TSTDR低剂量组(P＜0.01，P＜0.05)。结论：抑制脾脏TNF-α、IL-1β、IL-6的表达可能是TSTDR治疗AA的机制之一。
目的：觀察赤雹根總皂苷(TSTDR)對佐劑性關節炎(AA)大鼠脾髒指數和脾髒腫瘤壞死因子-α(TNF-α)、白細胞介素-1β(IL-1β)、白細胞介素-6(IL-6)錶達的影響。方法：雄性SD大鼠60隻隨機分為正常對照組，模型組，TSTDR低(40mg/kg/d)、中(80mg/kg/d)、高(160mg/kg/d)劑量組和雷公籐多苷組(12mg/kg/d)。大鼠右後足蹠部皮下註射弗氏完全佐劑0.1ml建立AA大鼠模型，成模後各用藥組大鼠分彆灌胃給予相應藥物21d。計算大鼠的脾髒指數，免疫組織化學染色法檢測各組大鼠脾髒TNF-α、IL-1β、IL-6的錶達。結果：TSTDR中、高劑量組大鼠的脾髒指數顯著低于模型組(P＜0.01，P＜0.05)。TSTDR各劑量組大鼠脾髒TNF-α、IL-1β、IL-6的錶達水平明顯低于模型組(P＜0.01，P＜0.05)；併且，TSTDR中劑量組、TSTDR高劑量組大鼠脾髒TNF-α、IL-1β、IL-6的錶達水平明顯低于TSTDR低劑量組(P＜0.01，P＜0.05)。結論：抑製脾髒TNF-α、IL-1β、IL-6的錶達可能是TSTDR治療AA的機製之一。
목적：관찰적박근총조감(TSTDR)대좌제성관절염(AA)대서비장지수화비장종류배사인자-α(TNF-α)、백세포개소-1β(IL-1β)、백세포개소-6(IL-6)표체적영향。방법：웅성SD대서60지수궤분위정상대조조，모형조，TSTDR저(40mg/kg/d)、중(80mg/kg/d)、고(160mg/kg/d)제량조화뢰공등다감조(12mg/kg/d)。대서우후족척부피하주사불씨완전좌제0.1ml건립AA대서모형，성모후각용약조대서분별관위급여상응약물21d。계산대서적비장지수，면역조직화학염색법검측각조대서비장TNF-α、IL-1β、IL-6적표체。결과：TSTDR중、고제량조대서적비장지수현저저우모형조(P＜0.01，P＜0.05)。TSTDR각제량조대서비장TNF-α、IL-1β、IL-6적표체수평명현저우모형조(P＜0.01，P＜0.05)；병차，TSTDR중제량조、TSTDR고제량조대서비장TNF-α、IL-1β、IL-6적표체수평명현저우TSTDR저제량조(P＜0.01，P＜0.05)。결론：억제비장TNF-α、IL-1β、IL-6적표체가능시TSTDR치료AA적궤제지일。
Objective:To study the effects of total saponins of Thladiantha dubia root (TSTDR) on spleen index and TNF-α, IL-1β, IL-6 expression in spleen of adjuvant arthritis (AA) rats.Methods:60 male SD rats were randomly divided into the following 6 groups with 10 rats in each group:normal control group, model group, TSTDR low dose (40 mg/kg/d) group, TSTDR middle dose (80 mg/kg/d) group, TSTDR high dose (160mg/kg/d) group and tripterygium glycoside group (12mg/kg/d).TheAArats’model was established by injecting Freund’s complete adjuvant into the plantar subcutaneous layer of right rear foot of rats, and then the rats in each drug group were lavaged with corresponding drugs for 21 days.The spleen index of rats in each group was calculated and immunohistochemical method was used to detect the TNF-α, IL-1β, IL-6 expression in spleen. Results:ThespleenindexofratsinTSTDRmiddleandhighdosegroupwereobviouslylowerthanthatofratsinmodelgroup(P<0.01, P<0.05).TheTNF-α, IL-1β, IL-6 expression in spleen of rats in eachTSTDR group were all significantly lower than model group (P<0.01, P<0.05);Moreover,TheTNF-α, IL-1β, IL-6 expression in spleen of rats inTSTDR middle and high dose group were significantly lower than TSTDR low dose group (P<0.01, P<0.05).Conclusions:Inhibition of TNF-α, IL-1βandIL-6expressioninspleenmaybeoneofthemechanismsofTSTDRfortreatingAA.
