火针疗法是一种独特的中医传统外治方法,具有以针代刀提脓泻毒等多种功效.非哺乳期乳腺炎是一种常见的难治性乳腺良性疾病,其病情复杂多变,易形成脓肿和窦道、瘘管,迁移难愈,适合火针治疗,但相关研究较少.在总结古今医家运用火针治疗非哺乳期乳腺炎临床经验的基础上,对火针治疗非哺乳期乳腺炎的适应证、禁忌证、操作方法及注意事项进行了规范.

非哺乳期乳腺炎是一组发生于乳房的慢性非细菌性炎症疾病,以乳房肿块、脓肿和窦道、瘘管为主要表现,病情反复发作,迁延难愈.中医外科内治法按照疾病初起、成脓、溃后3个不同阶段,确立消、托、补3个治疗原则,托法是其中最具代表性的特色疗法.该病以半阴半阳证最为常见.治疗上,阳证以清消为主,阴证以为温通为主,而对于半阴半阳证,托法则更为合适.从清托透邪法、托里透脓法、托里生肌法探讨托法在非哺乳期乳腺炎中的具体运用,治疗以托法为主,与他法联用,寓消于托,寓补于托.根据托法治疗非哺乳期乳腺炎的理论,在辨病辨证基础上,创立治疗成脓期和溃后期的"浆乳2号方",并结合临床病例对具体用药进行介绍.

目的:研究采用响应面法优化红景天抗氧化有效物质的提取工艺.方法:以乙醇浓度、提取时间、乙醇用量为主要影响因素,红景天苷提取率(％)、提取液体外DPPH清除率(％)和提取液体外总抗氧化能力为评价指标,采用3因素5水平响应面法对红景天抗氧化有效物质提取工艺进行优化.结果:Design-Expert软件优化得到的最佳提取工艺为,饮片加11倍体积46.60％乙醇溶液提取4.67 h,提取2次,合并提取液,浓缩,即得.该提取工艺下红景天苷提取率为1.12％,提取液DPPH清除率为89.13％,总抗氧化能力为1.39 mmol/L.结论:用响应面法优化得到的红景天抗氧化有效物质提取工艺简便易行,准确性和重现性好.

BACKGROUND:Gubenzhike recipe, a traditional Chinese herbal compound, was assumed to have a possible beneficial effect on COPD. This study was designed to elucidate the mechanism from the perspective of respiratory mucosal immunity.METHODS:COPD model was induced by exposure to cigarette smoke and LPS instillation in mice for 12 weeks. Animals were administered solution of Gubenzhike recipe by intragastric gavage daily for 4 weeks. After that, mice were sacrificed for lung function test and histological examination of lung tissues. The levels of IL-6 and IL-13 in serum, bronchoalveolar lavage fluid (BALF), and intestinal mucus were measured by ELISA. The KGF and KGFR in lung tissue were analysed by immunohistochemical staining, ELISA, and western blotting, and the mRNA expressions were assessed by PCR. γδT lymphocytes in the lungs were isolated and analysed by immunohistochemical staining and flow cytometry.RESULTS:Gubenzhike recipe improved the structure of airway and damage of lung tissue and also the respiratory status and lung function, reduced the content of IL-6 in serum and BALF and IL-13 in BALF and intestinal mucus, increased the proportion of γδT cells in lung tissue, and promoted the secretion of KGF and KGFR (P < 0.05).CONCLUSION:We for the first time demonstrated an experimental procedure for the isolation of γδT lymphocytes from lung tissue. This study suggested that Gubenzhike recipe could enhance the respiratory mucosal immunity which provided experimental evidence for its effects of reinforcing "wei qi" by means of strengthening vital qi, tonifying spleen and kidney, relieving cough, and reducing phlegm in TCM.

Saikosaponin A (SSa) is isolated from the dried root of Radix Bupleuri, an herb widely used in traditional Chinese medicine, exerting antitumor activities. The T helper cell type 1(Th1)/Th2 balance is associated with antitumor immunity in breast cancer. The present study aimed to investigate the effects of SSa on Th1/Th2 balance in breast cancer and to explore the underlying mechanisms. Breast cancer in rats was induced by intragastrical administration of 7,12-dimethyl-benz[a] anthracene once (100 mg/kg). At d(91), the rats suffering from tumors were randomly divided into three groups and treated with vehicle solution (control group), tamoxifen (TAM group), and SSa (SSa group) daily for 56 days, respectively. The tumor volume reduction ratio and tumor cell proliferation were detected to assess the antitumor effect of SSa. The positive staining numbers of CD8+ and CD4+ T cells infiltrated in breast tumors were measured by immunohistochemistry to evaluate the antitumor immunity of SSa. Cytokine levels in serum secreted by Th1 cells [interferon gamma (IFN-gamma), interleukin (IL)-12] and Th2 cells (IL-4, IL-10) were detected to evaluate Th1/Th2 balance. The related molecules of IL-12/signal transducers and activators of transcription 4 (STAT4) pathway were detected by immunohistochemistry staining, RT-PCR, and Western blot to explore the mechanisms of SSa. The results showed that, compared with the control group, SSa significantly inhibited tumor growth and tumor cell proliferation. SSa enhanced antitumor immunity, which was demonstrated as increased CD8+ T cells and CD4+ T cells infiltrated in tumors. SSa shifted Th1/Th2 balance toward Th1, which was confirmed as increased serum IFN-gamma and IL-12 levels, while decreased serum IL-4 and IL-10 levels. SSa increased IL-12, IL-12 receptor, and phosphorylated STAT4 expressions to promote Th1 differentiation. In conclusion, the present work suggested that SSa could inhibit breast cancer growth by shifting Th1/Th2 balance toward Th1. The underlying mechanism may involve activation of the IL-12/STAT4 pathway that induced Th1 differentiation.

目的:探讨延寿液通过调控炎症和维持胶原延缓臭氧吸入所诱导大鼠皮肤衰老的作用机制.方法:将48只大鼠按照随机数字表法分为对照组、模型组、维生素E组、延寿液低剂量组、延寿液中剂量组和延寿液高剂量组,每组各8只.对照组大鼠每天吸入新鲜空气10 h,模型组和各给药组大鼠每天吸入臭氧(1.2±0.2)ppm,10 h造模.检测各组大鼠血浆/肝肾组织总超氧化物歧化酶(T-SOD)和铜锌超氧化物歧化酶(CuZn-SOD)活力、血浆锰超氧化物歧化酶(Mn-SOD)活力,血清/肝肾组织丙二醛(malondialdeyde,MDA)含量,皮肤羟脯氨酸(Hyp)含量,苦味酸天狼星红染色定量皮肤胶原面积,免疫组织化学染色检测转化生长因子-β(transforming growth factor-β,TGF-β)表达,蛋白斑点测定皮肤基质金属蛋白酶-1(matrix metalloproteinase-1,MMP-1)表达变化.结果:与对照组比较,模型组大鼠血液T-SOD、Mn-SOD的活性及Hyp含量下降,MDA含量显著升高(P<0.01).与模型组比较,延寿液低剂量组、延寿液中剂量组和延寿液高剂量组T-SOD、Mn-SOD的活性显著升高,CuZn-SOD活性、MDA及Hyp含量显著降低,差异具有统计学意义(P<0.01).与对照组比较,模型组肝组织MDA含量升高,肾组织T-SOD、CuZn-SOD活力降低,MDA含量明显增高(P<0.01);与模型组比较,延寿液低剂量组肝MDA含量降低显著(P<0.01),延寿液低剂量组、中剂量组肾T-SOD活力显著升高(P<0.05),延寿液低剂量组肾MDA的含量显著降低(P<0.05);与对照组比较,模型组TGF-β1含量降低、皮肤MMP-1蛋白表达显著增高,差异有统计学意义(P<0.01);与模型组比较,维生素E组和延寿液低剂量组中TGF-β1含量升高、皮肤MMP-1的表达降低,差异具有统计学意义(P<0.05).结论:延寿液通过上调TGF-β1调控炎症,同时下调MMP-1维持胶原,具有延缓皮肤衰老的作用.

目的:观察希望液对衰老模型大鼠皮肤脂褐素沉积的影响及延缓皮肤衰老的药效.方法:采用吸入臭氧法复制大鼠衰老模型,各给药组分别灌胃给予阳性对照药(维生素E,13.5 mg·kg-1)及低、中、高剂量(225,450,900 mg·kg-1)希望液,模型组和正常对照组给予等量蒸馏水.检测大鼠血清总超氧化物歧化酶(T-SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)、丙二醛(MDA)含量;HE染色显示皮肤病变,形态计量表皮角质层体积比;三氯化铁-铁氰化钾染色显示皮肤脂褐素,形态计量表皮脂褐素沉积体积比.结果:与正常对照组比较,模型组大鼠血清T-SOD、CAT、GSH-Px水平及皮肤表皮角质层体积比显著降低(P<0.05),MDA水平和脂褐素沉积显著升高(P<0.05或P<0.01).与模型组比较,希望液能升高大鼠血清T-SOD、CAT、GSH-Px水平及皮肤表皮角质层体积比,降低MDA水平和脂褐素沉积;其中希望液各剂量组的T-SOD、MDA水平及脂褐素沉积、中、高剂量组的CAT水平、高剂量组的GSH-Px水平及皮肤表皮角质层体积比与模型组比较差异有统计学意义(P<0.05或P<0.01).结论:希望液通过抑制氧化应激损伤,减少表皮脂褐素沉积,延缓皮肤衰老.

目的 观察固本止咳中药对慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)模型小鼠肺功能及分泌型免疫球蛋白A (SIgA)的影响.方法 将150只小鼠使用完全随机方法分为5组,即空白对照组、模型对照组、高剂量中药组、中剂量中药组和低剂量中药组,每组30只.除空白对照组外,其余4组采用鼻腔滴入脂多糖(LPS)加熏香烟的方法建立COPD小鼠模型.中药组第141天开始予固本止咳中药0.036 g生药/mL(低剂量)、0.112 g生药/mL(中剂量)、0.22 g生药/mL(高剂量)各0.2 mL/d灌胃,空白对照组、模型对照组以同样方法予0.9％氯化钠溶液灌胃,均干预4周.造模期间观察小鼠的一般情况,用HE染色法观察肺组织形态学变化,检测各组肺功能指标,用酶联免疫吸附法检测血清、肺泡灌洗液(BALF)、肠灌洗液(ILF)中SIgA水平.结果 模型对照组肺组织符合COPD临床病理形态学改变,肺功能下降.与模型对照组比较,各中药组肺功能改善(P＜0.05),血清及ILF中SIgA水平低(P＜0.05),BALF中SIgA水平高(P＜0.05).结论 固本止咳中药可以提高CODP小鼠肺组织弹性及肺顺应性,改善肺功能状态;增加BALF的SIgA水平,改善呼吸道黏膜免疫功能;减少血清及ILF中SIgA的分泌,缓解全身炎性损伤程度.

Objective:To develop a HPLC method for the determination of the concentration of Pae in rat plasma,and to study the pharmacokinetics of Pae in different stages of hepatic precancerous lesion model.Methods:Rats were successful modeling after given diethylnitrosamine(DEN),given single Pae by oral,blood taken from orbital at different time points,determined concentration of Pae by UPLC,the pharmacokinetic parameters were calculated by WinNonlin software;the expression of Estrogen Sulfate Transferase (EST) protein in liver and kidney were detected by immunohistochemistry.Results:Low dose group of Pae:from d000-d028-d056-d112,AUC,Cmax increased in turn,CL,V,MRT decreased in turn;middle dose group of Pae:from d000-d028-d056-d112,AUC,Cmax increased in turn,V,MRT decreased in turn,from d000-d028-d056,CL decreased in turn,from d056-d112,CL increased;high dose group of Pae:from d000-d028-d05 6-d112,AUC,Cmax increased in turn,CL,V,MRT decreased in turn.EST increased in liver endothelial cells and renal epithelial cells,decreased in liver cells.Conclusion:A simple and specific HPLC method for the analysis of Pae was successfully developed and applied to a pharmacokinetic study in rat plasma.

目的 探究杞红液对臭氧吸入联合冰水浴诱导大鼠血管纤维化的影响.方法 运用臭氧复合冰水浴造模法,制作寒凝血瘀衰老大鼠模型,检测血清NOS、MPO活力,ET-1含量;运用Masson染色和免疫组化来观察杞红液对动脉血管纤维沉积的影响.结果 与对照组比较,模型组NOS活力降低(P＜0.05),MPO活力升高(P＜0.05),ET-1含量降低(P＜0.05),血管纤维沉积增加(P＜0.05),TGF-β1表达量升高(P＜0.05).与模型组比较,杞红液低、中、高剂量对上述指标、胶原纤维沉积、TGF-β1表达量有不同程度改善(P＜0.05).结论 杞红液可能是通过调节大鼠NOS和ET-1的表达含量,调节机体应激反应,改善血管内皮功能及改善血管纤维化来实现对血管的保护作用.

OBJECTIVE:To evaluate vitality principle in breast cancer rats by pharmacologically developing a model for anticancer surveillance.METHODS:The breast cancer in rats was replicated with 7,12-Dimethylbenz[a]anthracene (DMBA, i.g., 100 mg/kg) at d001. The anticancer surveillance was defined as the intervals between the primary sensitization and the first challenge stirred with complete Freund's adjuvant (CFA), the various intervals (k = 0.80) were dominated from d025 (600.00 h) to d095 (2288.82 h). The optimal surveillant status was confirmed with the median effective interval (EI50) from tumor volume regressive curve, for developing the pharmacodynamic model. The tumor and tumor infiltrating lymphocyte histopathology was used to confirm the immune surveillance being affected with CFA in breast cancer tumorigenesis. The availability of this model was confirmed with Shugan Liangxue prescription (SLP), from the vitality principle, and assured further from interleukin-12 levels.RESULTS:The regressive curve was set up between the intervals and tumor volumes, the EI50 in SLP-treated rats (1475.00 h, YSLP = 0.1026 + 0.8780/[1 + 10(27.1425-8.565x)]) was postponed, which was 1.87 multiple of the EI50 in CFA rats (791.40 h, y = -0.0525 + 0.9452/[1 + 10(30.4870-10.52x)], so did prepone the curve between the intervals and the immunological biomarker, serum interleukin-12 levels, the EI50 in SLP-treated rats (744.90 h, YSLP = -0.0145 + 0.7455/[1 + 10(52.09636-18.13x)]) be 0.78 multiple of the EI50 in CFA rats (960.10 h, YCFA = 0.2460 + 0.7270/[1 + 10 (-67.1546 + 22.52x)]), this immunological action being mediated the anticancer prognosis. Tumor histology was confirmed the more tumor infiltrating lymphocytes activated in SLP rats with CFA stirred immunity than rats only received CFA.CONCLUSION:The model for anticancer surveillance was pharmacologically established as the optimal interval (791.40 h) between the primary sensitization and the first challenge stirred with complete Freund's adjuvant. This available model was confirmed with SLP, from the vitality principle, for evaluating immunological effects against breast cancer.

Ethnopharmacological relevance: Qingdu granule (QDG), a traditional Chinese herbal prescription, had antitumor effect on breast cancer. However the underlying mechanism of QDG was unclear. The aim of this study: The present study aimed to investigate whether QDG could inhibit angiogenesis of breast cancer via acting on nuclear factor of activated T-cells (NFAT) signaling pathway. This was implicated in human umbilical vein endothelial cells (HUVECs) in vitro and breast cancer xenograft model in vivo. Materials and methods: The VEGF(165) (15.58 ng/mL) induced human umbilical vein endothelial cells (HUVECs) were treated with serum samples containing tamoxifen (TAM), tacrolimus (FK506), or QDG with three dosages. The migration and canalization capacities of HUVECs were evaluated by transwell migration and tube formation assay. In 72 h-cultured HUVECs, The gene expression, protein amount, and nuclear translocation of NFATc3 were measured. The anti-tumor and anti-angiogenic effects of QDG in vivo were investigated in breast cancer xenograft model. The serum VEGF levels, microvessel density, and protein expressions (immunohistochemistry and western blot) of VEGF, VEGFR2 and NFATc3 were detected. Results: The results showed that, QDG significantly inhibited HUVEC migration and tube formation. It down regulated NFATc3 gene expression, decreased NFATc3 protein amount, and reduced the ratio of NFATc3 nuclear translocation in HUVECs. In breast cancer xenograft model, QDG treatment significantly suppressed tumor growth, inhibited VEGF release, and decreased microvessel density. QDG reduced protein expressions of VEGF, VEGFR2 and NFATc3. Conclusion: The results suggested that QDG showed anti-angiogenic effects of breast cancer both in vitro and in vivo. The mechanism might be partially associated with inhibiting NFAT signaling pathway.

Objective:To observe the role of Luteolin after the infection of influenza virus (H1N1) in human lung cancer cell line (A549 cell line).Methods:The maxinum of non-toxic concentration (TC0) and the median toxic concentration (TC50) were detected by the cytopathogenic effect (CPE) of cells.Furthermore,The median inhibitory concentration (IC50) and treatment indexes (TI) in the best mode were calculated by Probit regression.Results:The median toxic concentration of Luteolin was 39.810 μg·mL-1,and maximum non-toxic concentration was 25 μg·mL-1;A significant inhibitory effect was shown when added luteolin from 12.5 to 25.0 μg·mL-1 after 48-60 h compared with the model without the drug.In addition,the best method against viral infection was adding Luteolin at 2 after cells infected and the best survival rate was (87.00±1.71) ％ with 25.0 μg·mL-1 of Luteolin.Under this condition,IC50 was 11.282 μg·mL-1,and TI was 3.528.Conclusion:Luteolin possesses the effect of anti-H1NI virus in vitro.

目的:探讨希望III号液对臭氧加重二乙基亚硝胺(DEN)致大鼠肝损伤的治疗作用.方法:48只雄性Wistar大鼠随机分为对照组、模型组、维生素E组、希望III号液低、中、高剂量组,每组8只.对照组吸入新鲜空气,腹腔注射(ip)生理盐水50 mg/kg;各造模组腹腔注射DEN 50 mg/kg,每周2次,同时吸入臭氧(0.65±0.12) ppm, 4 h/d,各组于造模2周后开始给药,其中对照组和模型组每天灌胃(ig)饮用水,各给药组同步灌胃维生素E(13.5 mg/kg)与希望III号液(45、90、180 mg/kg)治疗.给药8周后取大鼠血清和肝脏组织,检测大鼠血清转氨酶(ALT和AST)、谷胱甘肽S-转移酶(GST)、碱性磷酸酶(ALP)和丙二醛(MDA)、分型超氧化物歧化酶(CuZn-SOD、T-SOD)、谷胱甘肽过氧化物酶(GSH-Px)含量;肝脏组织常规HE染色、Masson染色观察组织形态;形态剂量肝细胞体积构成比、肝胶原纤维体积比.结果: 模型组大鼠血清ALT、AST、GST、ALP、MDA含量升高(P<0.01), CuZn-SOD、T-SOD和GSH-Px含量降低(P<0.01),肝细胞体积构成比增大(P<0.01),胶原纤维沉积增加(P<0.01).希望III号液能抑制大鼠血清ALT、AST、GST、ALP、MDA含量升高(P<0.01),回升CuZn-SOD、T-SOD和GSH-Px含量(P<0.01),回降肝细胞体积构成比和胶原纤维沉积增加(P<0.01). 结论:希望III号液可以改善肝损伤状态下肝脏功能,调节肌体氧化应激过程,延缓肝脏纤维化进程,对臭氧加重DEN致大鼠肝损伤有保护作用.

Objective: To investigate the pharmacological effect of Bupi Yichang (BPYX) pill on colonic contraction of rats and explore its underlying mechanism. Methods: The experiments were performed on colonic longitudinal smooth muscle strips (CLSMs) under isometric conditions. CLSMs suspended in tissue chambers were stimulated by KCl (80 mM) or acetylcholine (ACh, 0.1 mM), or exhausting intracellular Ca2+ and internal flow of extracellular Ca2+ to induce muscle contraction and their responses to different doses of BPYX pill were observed. After that, incubation with different inhibitors was conducted to verify its underlying mechanism. Results: Bupi Yichang pill dose-dependently and reversibly inhibited colonic contraction. The antispasmodic effect of BPYC pill was partially blocked by 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester hydrochloride (TMB-8, an intracellular Ca2+ antagonist, 500 μM), thapsigargin (a non-competitive inhibitor of the sarco/endoplasmic reticulum Ca2+ ATPase, 1 μM), and nifedipine (a voltage-dependent Ca2+ channel blocker, 10 μM) (P < .05). However, there were no significant difference after incubation with ethylene glycol tetraacetic acid (EGTA, a calcium chelating agent, 1 mM), 4-aminopyridine (4-AP, a potassium channel blocker, 50 μM), NG-nitro-l-arginine methyl ester (l-NAME, an inhibitor of nitric oxide synthase, 10 mM), methylene blue (an inhibitor of cyclic guanosine monophosphate, 10 μM) and apamin (a selective blocker of Ca2+-activated K+ channel, 0.1 μM) (P > .05). Conclusion: Bupi Yichang pill could inhibit colonic contraction of rats in vitro and its antispasmodic effect might be partially mediated by calcium channels.

Objective To discuss the influence of Qihong Fang (Wolfberry and Hawthorn Decoction) on heart in aged rats with cold-congealing and blood-stasis pattern.Methods SD rats (n =48) were divided randomly into normal control group,model group,vitamin E group (13.5 mg/kg),low-dose Qihong Fang group (45 mg/kg),mid-dose Qihong Fang group (90 mg/kg) and high-dose Qihong Fang group (180 mg/kg).The aged rat model of cold-congealing and blood-stasis pattern was established through 28-d ozone leading to aging and 14-d ice water leading to cold-congealing and blood-stasis pattern in other 5 groups except of control group.On the 29th d,the blood samples were collected from abdominal aorta for isolating serum and plasma,and heart was separated too.The vitalities of serum total superoxide dismutase (T-SOD),Cu-Zn SOD,Mn-SOD,catalase (CAT),glutathione peroxidease (GSH-PX),content of malondialdehyde (MDA),and prothrombin time (PT),activated partial thromboplastin time (APTT),thrombin time (TT) and fibrinogen (FIB) were detected.The morphologic changes of heart cells were observed after HE staining,fiber deposition quantity was observed after Masson staining,expression of transforming growth factor β1 (TGF-β1) was detected by using immunohistochemistry technique for reviewing aging model of cold-congealing and blood-stasis pattern,and protective effect of Qihong Fang on heart was observed in rats.Results Compared with normal control group,the vitalities of T-SOD,Cu-Zn-SOD,Mn-SOD,CAT and GSH-PX decreased significantly (P ＜ 0.05),MDA content increased significantly (P＜ 0.05,PT and APTT decreased significantly (P ＜ 0.05),and FIB content increased significantly (P ＜0.05) in model group.After Masson staining,morphometry observation by light microscope showed deposition of heart collagen fibers increased significantly (P ＜ 0.05),and expression of TGF-β1 increased significantly (P ＜ 0.05).Compared with control group,the vitalities of T-SOD,Cu-Zn-SOD,CAT and GSH-PX increased significantly (P ＜ 0.05),MDA content decreased significantly (P ＜ 0.05),PT and ATPP increased significantly (P ＜ 0.05),FIB content decreased significantly (P ＜ 0.05),deposition of heart collagen fibers decreased significantly (P ＜0.05),and expression of TGF-β1 decreased significantly (P ＜ 0.05) in mid-dose and high-dose Qihong Fang groups.Conclusion Qihong Fang has a protective effect on heart in aged rats with cold-congealing and blood-stasis pattern.

Objective To investigate the cardioprotective effect of Xiwang Ⅱ in mice exposed to passive smoking and its mechanism of action.Methods A total of 72 male Kunming mice were randomly divided into control group, model group, positive drug group, and low-, middle-, and high-dose Xiwang Ⅱ groups.The mice in the control group were exposed to laboratory air, and those in the model group were exposed to cigarette smoke for 45 consecutive days (3 hours a day).The drugs were administered since day 16 of exposure and the mice were sacrificed on day 45 to collect heart tissue.The level of malondialdehyde (MDA) in the heart was measured, as well as the activities of cardiac total superoxide dismutase (T-SOD),copper-zinc superoxide dismutase (Cu-ZnSOD), and myeloperoxidase (MPO).The histomorphological features of the heart were observed and the collagen fiber area in the heart was calculated.Immunohistochemistry was used to measure the expression of transforming growth factor-β1 (TGF-β1) in the heart.Results Compared withthe control group, the model group had significant reductions in the activity of Cu-ZnSOD and T-SOD (P<0.05) and significant increases in MPO activity, MDA level, cardiac muscle fibers, and TGF-β1 expression (all P<0.05).Compared with the model group, the low-, middle-, and high-dose Xiwang Ⅱ groups had significant increases in the activities of Cu-ZnSOD and T-SOD (P<0.05) and significant reductions in MPO activity, MDA level, cardiac muscle fibers, and TGF-β1 expression (all P<0.05).Conclusion Xiwang Ⅱ exerts its cardioprotective effect on mice exposed to passive smoking by regulating oxidative stress response in the heart.

Objective:To establish an analytical method for determination of Pae in tissues of hepatic precancerous lesion model rats by UPLC,and study the tissue distribution of Pae in rats.Methods:The concentration of Pae in rats tissues were determined by UPLC.Results:In control group,kidney had the highest tissue concentration of Pae,followed by stomach,small intestine,brain,liver,spleen,heart,lung;in model group,liver had the highest tissue concentration of Pae,followed by kidney,spleen,small intestine,stomach,heart,brain,lung.And its AUCall in model group was larger than that in control group.Conclusion:Compared with the control group,the content of Pae in model group increased.

Objective To observe the influence of pulmonary fibrosis in PM2.5 model mice with Bufei Huoxue(BFHX)capsule.Methods PM2.5 model mice was established by intranasal instillation of PM2.5 suspension.There were seven groups including blank control,low dose infected and treated with BFHX,middle dose infected and treated with BFHX,high dose infected and treated with BFHX.Pulmonary fibrosis level,IL-6,TNF-α in lung tissue were detected by MASSON staining and ELISA.Results PM2.5 model mice were successfully established.Pulmonary fibrosis gradually aggravated with increase of the infected dose.Bufei Huoxue capsule could reduce lung inflammatory reaction(P<0.05).Conclusion Bufei Huoxue capsule can reduce the pulmonary fibrosis level and lung inflammatory reaction with PM2.5 model mice.

Objective:To observe the role of luteolin and explore its mechanism after the infection of influenza A virus (H1N1) in human lung cancer cell line (A549 cell line).Methods:The chips were used to screen the differentially expressed genes which selected from the apoptotic signaling pathway.The mRNA expressions of Casp3,Casp8 and Myd88 were verified by qRT-PCR.Results:According to the gene chips,oseltamivir and luteolin could down-regulate the expressions of Casp3,Casp6,Casp7,Casp8,Casp9 and MYD88 compared with the virus-infected group.qRT-PCR experiments showed that luteolin could significantly decrease the expressions of Casp3,Casp8 and MYD88.Conclusion:When apoptosis of A549 cells infected by influenza virus in vitro were induced,luteolin could down-regulate the expressions of genes related to the apoptosis pathway,which could interfere the cell apoptosis induced by virus infection,so as to achieve the anti-virus action.