中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
Chinese Journal of Industrial Hygiene and Occupational Diseases
2015年
9期
689-692
,共4页
李红军%刘宝南%李鹏%冯玲吉%马海红%轩诗孟%曹永芝
李紅軍%劉寶南%李鵬%馮玲吉%馬海紅%軒詩孟%曹永芝
리홍군%류보남%리붕%풍령길%마해홍%헌시맹%조영지
大鼠%姜黄素%百草枯%细胞因子
大鼠%薑黃素%百草枯%細胞因子
대서%강황소%백초고%세포인자
Rat%Curcumin%Paraquat%Cytokine
目的 探讨姜黄素在不同治疗条件下对PQ中毒大鼠血清炎症相关细胞因子的影响.方法 将50只清洁级8周龄Wistar雄性大鼠随机分为高剂量(1 000 mg/kg)姜黄素+常规治疗组、低剂量(500 mg/kg)姜黄素+常规治疗组、单独高剂量(1 000 mg/kg)姜黄素治疗组、PQ单纯染毒组和空白对照组,分别在染毒后第1、3、5、7、14和21天检测大鼠血清中转化生长因子β1(TGF-β1)、肿瘤坏死因子(TNF-α)、白细胞介素6(IL-6)含量,HE染色观察肺组织病理变化.结果 与空白对照组相比,高剂量姜黄素+常规治疗组、低剂量姜黄素+常规治疗组、单独高剂量姜黄素治疗组以及PQ单纯染毒组大鼠血清中TGF-β1、TNF-α和IL-6含量明显升高,差异均有统计学意义(P<0.05),其高峰出现在染毒后第14天.与PQ单纯染毒组比较,单独高剂量姜黄素治疗组大鼠血清中TGF-β1、TNF-α和IL-6含量明显降低,差异有统计学意义(P<0.05).染毒后第21天,高剂量姜黄素+常规治疗组大鼠血清中TGF-β1、TNF-α和IL-6含量与低剂量姜黄素+常规治疗组比较,差异无统计学意义(P>0.05).肺组织HE染色结果显示,高剂量姜黄素+常规治疗组、低剂量姜黄素+常规治疗组、单独高剂量姜黄素治疗组、PQ单纯染毒组大鼠第21天大量肺纤维化形成,但单独高剂量姜黄素治疗组明显轻于PQ单纯染毒组.结论 姜黄素可明显降低大鼠炎症反应水平,改善肺组织病理变化,抑制并延缓机体损伤的发生发展.
目的 探討薑黃素在不同治療條件下對PQ中毒大鼠血清炎癥相關細胞因子的影響.方法 將50隻清潔級8週齡Wistar雄性大鼠隨機分為高劑量(1 000 mg/kg)薑黃素+常規治療組、低劑量(500 mg/kg)薑黃素+常規治療組、單獨高劑量(1 000 mg/kg)薑黃素治療組、PQ單純染毒組和空白對照組,分彆在染毒後第1、3、5、7、14和21天檢測大鼠血清中轉化生長因子β1(TGF-β1)、腫瘤壞死因子(TNF-α)、白細胞介素6(IL-6)含量,HE染色觀察肺組織病理變化.結果 與空白對照組相比,高劑量薑黃素+常規治療組、低劑量薑黃素+常規治療組、單獨高劑量薑黃素治療組以及PQ單純染毒組大鼠血清中TGF-β1、TNF-α和IL-6含量明顯升高,差異均有統計學意義(P<0.05),其高峰齣現在染毒後第14天.與PQ單純染毒組比較,單獨高劑量薑黃素治療組大鼠血清中TGF-β1、TNF-α和IL-6含量明顯降低,差異有統計學意義(P<0.05).染毒後第21天,高劑量薑黃素+常規治療組大鼠血清中TGF-β1、TNF-α和IL-6含量與低劑量薑黃素+常規治療組比較,差異無統計學意義(P>0.05).肺組織HE染色結果顯示,高劑量薑黃素+常規治療組、低劑量薑黃素+常規治療組、單獨高劑量薑黃素治療組、PQ單純染毒組大鼠第21天大量肺纖維化形成,但單獨高劑量薑黃素治療組明顯輕于PQ單純染毒組.結論 薑黃素可明顯降低大鼠炎癥反應水平,改善肺組織病理變化,抑製併延緩機體損傷的髮生髮展.
목적 탐토강황소재불동치료조건하대PQ중독대서혈청염증상관세포인자적영향.방법 장50지청길급8주령Wistar웅성대서수궤분위고제량(1 000 mg/kg)강황소+상규치료조、저제량(500 mg/kg)강황소+상규치료조、단독고제량(1 000 mg/kg)강황소치료조、PQ단순염독조화공백대조조,분별재염독후제1、3、5、7、14화21천검측대서혈청중전화생장인자β1(TGF-β1)、종류배사인자(TNF-α)、백세포개소6(IL-6)함량,HE염색관찰폐조직병리변화.결과 여공백대조조상비,고제량강황소+상규치료조、저제량강황소+상규치료조、단독고제량강황소치료조이급PQ단순염독조대서혈청중TGF-β1、TNF-α화IL-6함량명현승고,차이균유통계학의의(P<0.05),기고봉출현재염독후제14천.여PQ단순염독조비교,단독고제량강황소치료조대서혈청중TGF-β1、TNF-α화IL-6함량명현강저,차이유통계학의의(P<0.05).염독후제21천,고제량강황소+상규치료조대서혈청중TGF-β1、TNF-α화IL-6함량여저제량강황소+상규치료조비교,차이무통계학의의(P>0.05).폐조직HE염색결과현시,고제량강황소+상규치료조、저제량강황소+상규치료조、단독고제량강황소치료조、PQ단순염독조대서제21천대량폐섬유화형성,단단독고제량강황소치료조명현경우PQ단순염독조.결론 강황소가명현강저대서염증반응수평,개선폐조직병리변화,억제병연완궤체손상적발생발전.
Objective To explore the mechanism of paraquat (PQ) poisoning and to observe the changes in inflammatory cytokines in PQ-exposed rats treated in different ways.Methods Fifty 8-week-old clean male Wistar rats were randomly divided into high-dose curcumin plus conventional treatment group,low-dose curcumin plus conventional treatment group,high-dose curcumin group,PQ poisoning group,and blank control group.On days 1,3,5,7,14,and 21 after PQ exposure,serum levels of transforming growth factor-β1 (TGF-β1),tumor necrosis factor-α (TNF-α),and interleukin-6 (IL-6) were measured.The pathological changes in lung tissue were evaluated by HE staining.Results Compared with the blank control group,the high-dose curcumin plus conventional treatment group,low-dose curcumin plus conventional treatment group,high-dose curcumin group,and PQ poisoning group had significantly increased serum levels of TGF-β1,TNF-α,and IL-6 (P<0.05),and the three cytokines in each group reached peak levels on day 14 after exposure.Compared with the PQ poisoning group,the high-dose curcumin group had significantly reduced serum levels ofTGF-β1,TNF-α,and IL-6 (P<0.05).On day 21 after exposure,there were no significant differences in serum levels of TGF-β1,TNF-α,and IL-6 between the high-dose curcumin plus conventional treatment group and the low-dose curcumin plus conventional treatment group (P>0.05).The HE staining revealed alveolar inflammatory changes on days 1 ~7 and massive pulmonary fibrosis on days 14~21 in the high-dose curcumin plus conventional treatment group,low-dose curcumin plus conventional treatment group,high-dose curcumin group,and PQ poisoning group,but the above changes were milder in the high-dose curcumin group than in the PQ poisoning group.Conclusion For rats with PQ poisoning,curcumin can significantly reduce inflammatory response and pathological changes in lung tissue and inhibit and delay the development and progression of body injury.