We aimed to explore the anti-infammatory bactivity of mollugin extracted from Rubia cordifolia L,a traditional Chinese medicine,on dextran sulfate sodium(DSS)-induced ulcerative colitis(UC)in mice.Thirty C57BL/6 mice ...We aimed to explore the anti-infammatory bactivity of mollugin extracted from Rubia cordifolia L,a traditional Chinese medicine,on dextran sulfate sodium(DSS)-induced ulcerative colitis(UC)in mice.Thirty C57BL/6 mice were divided into a control group(n=6),a model group(n=6),and three experimental groups(40,20,10 mg/kg of mollugin,n=6 each).DSS solution(3%)was given to mice in the model group and experimental groups from day 4 to day 10 to induce the mouse UC model.Mice in the experimental groups were intragastrically administrated mollugin from day 1 to day 10.Animals were orally given distilled water in the control group for the whole experiment time and in the model group from day 1 to day 3.The changes in colon pathology were detected by hematoxylin and eosin(HE)staining.Interleukin-1β(IL-1β)in the serum,and tumor necrosis factor-α(TNF-α)and interferon-γ(IFN)in the tissues were measured by enzyme linked immunosorbent assay.Expression levels of Toll-like receptor 4(TLR4)and myeloid differentiation factor 88 in the colon tissues were detected by immunohistochemistry.Results showed that mollugin could significantly reduce weight loss and the disease activity index in the DSS-induced UC mouse model.HE examinations demonstrated that mollugin treatment effectively improved the histological damage(P<0.05).The overproduction of IL-Iβand TNF-α was remarkably inhibited by mollugin treatment at doses of 20 and 40 mg/kg(P<0.05).Additionally,the levels of TLR4 in colon tissues were significantly reduced in mollugin-treated groups compared with the DSS group.Our findings demonstrated that mollugin ameliorates DSS-induced UC by inhibiting the production of pro-inflammatory chemocytokines.展开更多
目的:通过大叶茜草素干预小鼠air-pouch模型,探讨大叶茜草素对钛颗粒诱导的人工关节无菌性松动的抑制作用及其发生机制。方法:体重25~30 g BALB/c小鼠72只,随机分为6组,分别为空白组(A组)、颗粒组(B组)、低剂量组(C组)、中剂量组(D组)...目的:通过大叶茜草素干预小鼠air-pouch模型,探讨大叶茜草素对钛颗粒诱导的人工关节无菌性松动的抑制作用及其发生机制。方法:体重25~30 g BALB/c小鼠72只,随机分为6组,分别为空白组(A组)、颗粒组(B组)、低剂量组(C组)、中剂量组(D组)、高剂量组(E组)、溶液对照组(F组),小鼠air-pouch模型构建成功后,运用大叶茜草素对实验各组进行干预,连续14天后,收集气囊囊壁进行大体观察、HE染色、RT-PCR及ELISA检测。结果:小鼠都存活至实验结束,大体观察见A组气囊炎症反应轻,B、C、D、E、F组气囊炎症反应较重,其中B、F组最重,C、D、E组较弱,且D组较C、E组最弱。实验室检测发现,B、F组囊壁炎性细胞密度及TNF-α、IL-1β表达无差异(P>0.05);B、F组囊壁炎性细胞密度及TNF-α、IL-1β表达均较A组明显增加(P<0.05);C、D、E组囊壁炎性细胞密度及TNF-α、IL-1β表达均低于B、F组(P<0.05),其中D组最低,且均高于A组(P<0.05)。结论:钛颗粒能在小鼠air-pouch模型中造成和人工关节无菌性松动类似的炎症反应,大叶茜草素能有效抑制这种炎症反应,从而为临床运用药物抑制人工关节无菌性松动的发生及发展带来新的曙光。展开更多
基金This work was supported by the National Natural Science Foundation of China(No.81703380)the Natural Science Foundation of Hubei Province(No.2017CFB782)+1 种基金the Scientific Research Project of Health and Family Planning Commission of Hubei Province(No.WJ2017M077)the Applied Basic Research Project of Wuhan Science and Technology Bureau(No.2017060201010215).
文摘We aimed to explore the anti-infammatory bactivity of mollugin extracted from Rubia cordifolia L,a traditional Chinese medicine,on dextran sulfate sodium(DSS)-induced ulcerative colitis(UC)in mice.Thirty C57BL/6 mice were divided into a control group(n=6),a model group(n=6),and three experimental groups(40,20,10 mg/kg of mollugin,n=6 each).DSS solution(3%)was given to mice in the model group and experimental groups from day 4 to day 10 to induce the mouse UC model.Mice in the experimental groups were intragastrically administrated mollugin from day 1 to day 10.Animals were orally given distilled water in the control group for the whole experiment time and in the model group from day 1 to day 3.The changes in colon pathology were detected by hematoxylin and eosin(HE)staining.Interleukin-1β(IL-1β)in the serum,and tumor necrosis factor-α(TNF-α)and interferon-γ(IFN)in the tissues were measured by enzyme linked immunosorbent assay.Expression levels of Toll-like receptor 4(TLR4)and myeloid differentiation factor 88 in the colon tissues were detected by immunohistochemistry.Results showed that mollugin could significantly reduce weight loss and the disease activity index in the DSS-induced UC mouse model.HE examinations demonstrated that mollugin treatment effectively improved the histological damage(P<0.05).The overproduction of IL-Iβand TNF-α was remarkably inhibited by mollugin treatment at doses of 20 and 40 mg/kg(P<0.05).Additionally,the levels of TLR4 in colon tissues were significantly reduced in mollugin-treated groups compared with the DSS group.Our findings demonstrated that mollugin ameliorates DSS-induced UC by inhibiting the production of pro-inflammatory chemocytokines.
文摘目的:通过大叶茜草素干预小鼠air-pouch模型,探讨大叶茜草素对钛颗粒诱导的人工关节无菌性松动的抑制作用及其发生机制。方法:体重25~30 g BALB/c小鼠72只,随机分为6组,分别为空白组(A组)、颗粒组(B组)、低剂量组(C组)、中剂量组(D组)、高剂量组(E组)、溶液对照组(F组),小鼠air-pouch模型构建成功后,运用大叶茜草素对实验各组进行干预,连续14天后,收集气囊囊壁进行大体观察、HE染色、RT-PCR及ELISA检测。结果:小鼠都存活至实验结束,大体观察见A组气囊炎症反应轻,B、C、D、E、F组气囊炎症反应较重,其中B、F组最重,C、D、E组较弱,且D组较C、E组最弱。实验室检测发现,B、F组囊壁炎性细胞密度及TNF-α、IL-1β表达无差异(P>0.05);B、F组囊壁炎性细胞密度及TNF-α、IL-1β表达均较A组明显增加(P<0.05);C、D、E组囊壁炎性细胞密度及TNF-α、IL-1β表达均低于B、F组(P<0.05),其中D组最低,且均高于A组(P<0.05)。结论:钛颗粒能在小鼠air-pouch模型中造成和人工关节无菌性松动类似的炎症反应,大叶茜草素能有效抑制这种炎症反应,从而为临床运用药物抑制人工关节无菌性松动的发生及发展带来新的曙光。
