Pseudo-allergic reaction is an allergic reaction mediated by nonimmunoglobulin E (IgE), which does not require prior contact with antigen sensitization and directly leads to mast cell degranulation. Daphnetin (DAP) is known for its anti-inflammatory effects, but there are few studies on the effect of DAP on pseudo-allergy and its mechanism. To investigate the effect of DAP on pseudo-allergy and its mechanism, we inflicted pseudo-allergy on RBL-2H3 cells using C48/80 in vitro. Moreover, to assess the antipseudo-allergy effect of C48/80 in vivo, mouse models of local anaphylaxis, systemic anaphylaxis, and itch were used. The in vitro results show that DAP in-hibits degranulation and chemokine release; furthermore, DAP reduced the activation of the PLC-IP3R and MAPK signaling pathways induced by C48/80. Additionally, our in vivo results showed that DAP inhibited C48/80-induced local anaphylaxis and inhibited eosinophil aggregation, vasodilation and mast cell degranulation. In systemic anaphylaxis, DAP inhibits the decrease in body temperature and reduces the release of His, TNF-a and IL-8. In C48/80-induced itch, the number of scratches in mice was reduced. Our results demonstrate that DAP can play a suppressive role in the pseudo-allergy induced by C48/80, providing information for the cure of disorders linked to pseudo-allergic reactions.

Atopic dermatitis (AD) is a common chronic inflammatory skin disease. Bisdemethoxycurcumin (BDMC) is an ingredient from the rhizome of the traditional Chinese herbal medicine turmeric. BDMC has been reported to have important pharmacological properties, such as anti-inflammatory, antioxidant, antitumor and antiproliferative activities. However, its effect on atopic dermatitis has not been reported. The purpose of our study was to demonstrate the effectiveness of BDMC on TNF-α/IFNγ-stimulated HaCaT cells and on 2,4-dinitrochlorobenzene (DNCB)-induced AD mice. Our studies showed in vitro that BDMC was able to significantly inhibit the mRNA expression of chemokines and cytokines in TNF-α/IFN-γ-stimulated HaCaT cells and alleviate their inflammatory response. Our studies found in vivo that BDMC was able to significantly improve the symptoms of DNCB-induced AD skin lesions, decrease the number of scratches, ear thickness, and spleen index, improve inflammatory cells and mast cell infiltration and decrease skin thickness. Moreover, it was also able to inhibit the mRNA expression levels of chemokines and inflammatory cytokines and the activation of the MAPK and NF-κB signaling pathways. Thus, the results indicated that BDMC can improve atopic dermatitis in mice and that further clinical studies are warranted on its treatment of AD.

Bisdemethoxycurcumin (BDMC) is an important ingredient derived from turmeric in addition to curcumin. It has been reported that BDMC can be used to treat mast cell-mediated allergic diseases. In the present study, a food allergy (FA) murine model sensitized by intraperitoneal injection followed by oral challenge with ovalbumin (OVA) was established. BDMC was orally administered at 100 and 200 mg/kg for 11 days in the challenge phase to treat OVA-induced FA mice. FA symptoms such as diarrhea score, anaphylactic symptom score and rectal temperature were recorded. Intestinal tissue was also observed by hematoxylin and eosin staining. In addition, other allergic indicators were also analyzed by ELISA and western blot analysis. The present study demonstrated that BDMC could suppress the decreases in rectal temperature, diarrhea and anaphylactic symptoms in FA mice. BDMC could also ameliorate the inflammation of intestinal tissues in FA mice. BDMC not only decreased the production of OVA-specific immunoglobulin (OVA-sIg)E, IgG1, histamine, mouse mast cell protease-1, diamine oxidase, cytokines (IL-4, IL-5 and IL-13) but increased cytokines interferon-γ production. The protein expression results showed that the levels of Gata-3 were decreased but T-bet levels were increased. Furthermore, compared with the OVA group, phosphorylated (p)-p38, p-JNK, p-ERK and p-NF-κBp65 levels were decreased and p-IκBα level was increased. In conclusion, the results showed that BDMC possessed a protective effect on FA. Furthermore, BDMC was able to regulate the T-helper cells (Th)1/Th2 immune balance and inhibit the activation of MAPK and NF-κB pathways in FA mice.

Pseudoallergic reactions are hypersensitivity reactions mediated by an IgE-independent mechanism. Since allantoin (AT)-mediated pseudoallergy has not been studied, in this study, our objective is to investigate the anti-pseudoallergy effect of AT and its underlying mechanism. In vitro, β-hexosaminidase (β-Hex) and histamine (HIS) release assays, inflammatory cytokine assays, toluidine blue staining, and F-actin microfilament staining were used to evaluate the inhibitory effect of AT in RBL-2H3 cells stimulated with Compound 48/80 (C48/80). Western blot analysis is further performed to investigate intracellular calcium fluctuation-related signaling pathways. In vivo, Evans Blue extraction, paw swelling, and the diameter of Evans Blue extravasation were evaluated, and skin tissues are examined for histopathological examination in mice with passive cutaneous anaphylaxis (PCA) induced by C48/80. Body temperature is measured, and the levels of cytokines are further determined by ELISA kits in mice with active systemic anaphylaxis (ASA) induced by C48/80. The results show that AT dose-dependently inhibited degranulation in C48/80-stimulated RBL-2H3 cells by inhibiting β-Hex and HIS release, reducing the levels of TNF-α, IL-8, and MCP-1, inhibiting shape changes due to degranulation and disassembling the F-actin cytoskeleton. Furthermore, AT dose-dependently inhibits the phosphorylation of PLCγ and IP3R. In vivo, AT decreased Evans Blue extravasation, paw swelling, and the diameter of Evans Blue extravasation and significantly ameliorate pathological changes and mast cell degranulation in C48/80-induced PCA. Furthermore, AT help the mice recover from the C48/80-induced decrease in body temperature and decreased the levels of cytokines in C48/80-treated ASA mice. Our results indicate that allantoin inhibits compound 48/80-induced pseudoallergic reactions. AT has the potential to be used in IgE-independent anti-allergic and anti-inflammatory therapies.

Berberine (BBR) has been reported to have potent anticancer activity and can increase the anticancer effects of chemotherapy drugs. The present study aims to investigate whether BBR and cisplatin (DDP) exert synergistic effects on the osteosarcoma (OS) MG-63 cell line. In the present study, MG-63 cells were treated with BBR and DDP alone or in combination. The effects of these therapeutics on cell viability, colony formation, migration, invasion, nuclear morphology, apoptosis, and the cell cycle, as well as their role in regulating the expression of proteins related to apoptosis, the cell cycle, and the mitogen-activated protein kinase (MAPK) pathway, were determined. The results demonstrated that BBR or DDP significantly inhibited the proliferation of MG-63 cells in a dose- and time-dependent manner. The combination treatment of BBR and DDP exerted a prominent inhibitory effect on proliferation and colony formation. Furthermore, the results showed that the combination treatment of BBR and DDP enhanced the inhibition of cell migration and invasion and reversed the changes in nuclear morphology. The results showed that the combination treatment of BBR and DDP induced apoptosis and cell cycle arrest in the G0/G1 phase. Mechanistically, the combination treatment of BBR and DDP inhibited the expression of MMP-2/9, Bcl-2, CyclinD1, and CDK4, enhanced the expression of Bax and regulated the activity of the MAPK pathway. Collectively, our data suggest that the combination therapy of BBR and DDP markedly enhanced OS cell death.

目的 探究稳尿胶囊对BOO大鼠膀胱过度活动症的治疗作用及其机制研究.方法 选取雌性SD大鼠60只,按体重随机分为假手术组6只,BOO模型组14只,阳性对照托特罗定(0.5mg/kg)组10只,稳尿胶囊高、中、低剂量(5.4、2.7、1.35mg/kg)组各10只.采用膀胱梗阻(BOO)模型复制膀胱过度活动症,造模的同时开始给药,每日1次,连续6周.末次给药2h后行膀胱造瘘术测定大鼠尿流动力学参数,记录PT及MP,收集UV及RV,计算TUV,收集尿液上清测定尿液NGF.取膀胱组织并观察膀胱组织形态学变化,称膀胱湿重,计算膀胱指数.取膀胱组织上清液测定IL-1β、SOD、MDA含量.结果 BOO模型大鼠的MP升高,膀胱湿重、膀胱指数升高(P<0.01),RV增多,UV降低(P<0.01);膀胱组织发生明显病变.尿液NGF、膀胱组织上清液IL-1β、MDA含量升高,SOD含量下降(P<0.01,P<0.05).与模型组相比,稳尿胶囊高剂量组和阳性对照组大鼠MP下降,RV减少、UV增多(P<0.01),膀胱湿重及膀胱指数减小(P<0.01),膀胱病变程度减轻.尿液NGF、膀胱组织上清液IL-1β、MDA含量下降,SOD含量升高(P<0.01,P<0.05).结论 稳尿胶囊可以改善BOO大鼠膀胱过度活动症状,可能是通过调节膀胱尿流动力学参数、减少膀胱刺激因素、降低膀胱氧化损伤而发挥作用.

目的 探讨稳尿胶囊对环磷酰胺诱导的大鼠膀胱过度活动症的治疗作用及其机制研究.方法 采用大鼠腹腔注射环磷酰胺(75mg/kg),每3日注射1次,共4次,建立大鼠膀胱过度活动症模型.造模后1h分别灌胃给予不同浓度稳尿胶囊高、中、低剂量(1.35、2.7、5.4mg/kg)和阳性对照托特罗定片(0.5mg/kg),每日1次,连续给药14天.实验期间观察大鼠一般状态.末次给药2h后检测大鼠尿流动力学参数(排尿压峰值,排尿基础压力,排尿间隔时间),测量膀胱剩余尿量.实验结束后称量膀胱湿重,计算膀胱指数.测量血清中NGF含量,测量膀胱组织上清液中SOD、MDA、IL-1β含量.结果 实验期间造模大鼠体重减轻,毛发脱落,口鼻出血,精神萎靡.与正常组相比,模型组大鼠排尿间隔时间缩短、排尿压峰值降低、膀胱剩余尿量增多、膀胱指数升高,均有显著性差异(P<0.01),体内NGF、MDA、IL-1β含量增加(P<0.01,P<0.05),SOD含量显著减少(P<0.01);与模型组比较,稳尿胶囊高剂量组和阳性对照组可延长排尿间隔时间、升高排尿压峰值、使膀胱残余尿量减少,均有显著性差异(P<0.01),可降低膀胱指数(P<0.05),降低体内NGF、MDA、IL-1β含量(P<0.01,P<0.05),显著升高SOD含量(P<0.01).结论 稳尿胶囊对环磷酰胺诱导的大鼠膀胱过度活动症具有治疗作用,其机制可能与改善尿流动力学指标及降低体内NGF、MDA、IL-1β含量及增加SOD含量有关.

目的 探讨益肾降浊胶囊对慢性肾功能衰竭(简称慢性肾衰)大鼠的治疗作用.方法 采用阳离子化牛血清白蛋白造成大鼠膜性肾病诱发慢性肾衰后,造模后的大鼠随机分为5组,即空白对照组、模型组、阳性药物肾衰宁组、益肾降浊胶囊高、中、低剂量组.每天定时定量灌胃给予药物,空白对照组组和模型组灌胃给予等量生理盐水.给药治疗6周后,观察各组大鼠的一般状态,测定各组大鼠24h尿蛋白量,测定大鼠血清中肌酐(Scr)及尿素氮(BUN)含量;观察肾脏组织病理变化的情况,检测超氧化物歧化酶(SOD)的活性和丙二醛(MDA)含量.结果 与模型组比较,通过益肾降浊胶囊治疗能够有效改善慢性肾衰大鼠的一般生存状态,显著降低大鼠24h尿蛋白量、血清肌酐(Scr)、尿素氮(BUN)的含量.病理结果显示,益肾降浊胶囊可缓解慢性肾衰大鼠的肾小球硬化及炎性细胞浸润.益肾降浊胶囊能够有效的增加CRF大鼠的肾脏组织SOD活性并降低MDA含量.结论 益肾降浊胶囊能够有效的治疗大鼠慢性肾功能衰竭.

目的 探讨组方优化的阳和胶囊对碘乙酸钠诱导的大鼠骨关节炎的治疗作用及其机制研究.方法 采用大鼠膝关节腔内注射4％碘乙酸钠溶液0.1 ml,连续注射7天,建立大鼠骨关节炎模型.于造模后分别灌胃给予组方优化的阳和胶囊高、中、低剂量及阳性对照双醋瑞因胶囊(8.0mg/kg),每日1次,连续给药4周.实验期间每周测定大鼠膝关节肿胀度.实验结束后测定大鼠膝关节灌洗液中NO、PGE-2含量,血清中IL-1β、TNF-α含量,及软骨组织中MMP-1、MMP-13含量.结果 实验期间模型组大鼠膝关节显著肿胀(P<0.01),各给药组与模型组相比均有不同程度缓解.组方优化的阳和胶囊高、中剂量组能够显著降低膝关节灌洗液中NO、PGE-2含量(P<0.01)、显著降低血清中IL-1β、TNF-α含量(P<0.01)明显降低软骨组织中MMP-1、MMP-13含量(P<0.05).结论 组方优化的阳和胶囊对碘乙酸钠诱导的大鼠骨关节炎具有治疗作用,其机制可能与降低膝关节灌洗液及血清中NO、PGE-2、IL-1β、TNF-α水平及软骨组织中MMP-1、MMP-13含量有关.

目的 探讨组方优化的阳和胶囊对木瓜蛋白酶诱导的大鼠骨关节炎的治疗作用及其作用机制.方法 采用大鼠膝关节腔内注射10％木瓜蛋白酶和0.03mol/L L-半胱氨酸混合溶液建立大鼠骨关节炎模型.于造模后分别灌胃给予组方优化的阳和胶囊高、中、低剂量及阳性药盐酸氨基葡萄糖(0.13g/kg),每日1次,连续4周.实验期间观察大鼠一般状态,每周测定大鼠膝关节肿胀度.实验结束后测定大鼠膝关节灌洗液中IL-1β、IL-6、TNF-α含量,及关节滑膜组织中糖胺多糖(GAGs)含量.结果 实验期间模型组大鼠膝关节显著肿胀(P<0.01),各给药组与模型组相比均有不同程度缓解.组方优化的阳和胶囊高、中剂量组能够显著降低膝关节灌洗液中IL-1β、IL-6、TNF-α的含量(P<0.01),显著增加关节滑膜组织中GAGs含量(P<0.01).结论 组方优化的阳和胶囊对木瓜蛋白酶诱导的大鼠骨关节炎具有治疗作用,其机制可能与降低膝关节灌洗液中IL-1β、IL-6、TNF-α的水平和增加关节滑膜组织中GAGs的含量有关.

A new ocotillol-type ginsenoside, namely 12-one-pseudoginsenoside F11 (12-one-PF11), was isolated from stems and leaves of Panax quinquefolium, whose structure was elucidated 6-O-[α-L-rhamnopyranosyl-(1-2)-β-D-glucopyranosyl]-dammar-12-one-20S,24R-epoxy-3β,6α,25-triol. 12-one-PF11 significantly suppressed hydrogen peroxide induced oxidative stress in human lung carcinoma A549 cells. As compared with model group, 12-one-PF11 improved cell viability of A549 cells in a dose-dependent manner, and significantly decreased the generation of malondialdehyde (MDA) and increased production of superoxide dismutase (SOD) and glutathione (GSH) and protein expression levels of nuclear related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in A549 cells.

目的 探讨益肾降浊胶囊对腺嘌呤诱导的慢性肾衰大鼠的肾脏保护作用.方法 采用灌胃给与腺嘌呤法建立大鼠慢性肾衰(CRF)模型,造模后每日1次连续灌胃给予益肾降浊胶囊.4周后,测定各组大鼠24h尿量、24h尿蛋白含量,称取大鼠体质量、肾重并计算肾指数,测定大鼠血清中肌酐(Scr)及尿素氮(BUN)含量,并在光镜下观察肾脏组织变化情况.结果 与对照组相比,模型组大鼠生长构建期间生长状态明显变差,体重增长缓慢.与CRF模型组大鼠相比,益肾降浊胶囊给药组的大鼠体重增加明显,大鼠血清中Scr、BUN及尿液中24h尿蛋白水平显著降低.病理分析结果显示,肾脏组织结构的紊乱、肾小球固缩,炎性细胞浸润、肾间质纤维化症状明显改善.结论 益肾降浊胶囊能够有效的治疗腺嘌呤所致的大鼠慢性肾功能衰竭.

Objective To explore the therapeutic effect of Qishao Granule on acetic acid-induced ulcerative colitis in mice. Methods The model of ulcerative colitis in mice was established by acetic acid enema. Qishao granules (14.0 g/kg, 7.0 g/kg, 3.5 g/kg) and salazosulfadimidine (SASP, 300 mg/kg) were given orally once a day for 7 days. The effects of Qishao Granules on ulcerative colitis in mice were evaluated by the changes of colon length and weight, pathological changes of HE staining, contents of IL-1β, TNF-α, MPO, SOD and NO in colon tissue. Results Qishao Granules in high and middle dose groups could significantly inhibit acetic acid-induced shortening of colon length, increase of intestinal weight, increase SOD activity in colon tissue, and decrease the contents of IL-1β, TNF-α, MPO and NO.Conclusion Qishao Granule has therapeutic effect on ulcerative colitis induced by acetic acid enema in mice. Its possible mechanism is related to increasing SOD activity and decreasing the contents of IL-1β, TNF-α, MPO and NO in mice with ulcerative colitis.

To study the therapeutic effect of Shenfukang tablet on membranous glom erulo-nephritis in rats.73 Wistar rats were randomly divided into normal control group, model control group, positive drug group, high dose Shenfukang tablet group, middle dose Shen fukang tablet group and low dose Shenfukang tablet group. The model of membranous glomerulo nephritis was induced by cationic bovine serum albumin injection into the tail vein of rats in other groups except the normal control group. At the end of the experiment, the amount of 24 h urine protein, serum creatinine (Scr) , urea nitrogen (BUN) , total protein (TP) and albumin (Alb) content were measured in rats. The pathological state of kidney was observed by hematoxyli n-eosin staining.Compared with the model control group, In the high-dose Shenfu-kang table group and middle-dose group, the urine protein content and the level of serum Scr (P < 0.01) , BUN (P < 0.05) were significantly decreased, and the level of TP (P < 0.05) and Alb (P < 0.01) were increased. Light microscopic examination of Shenfukang tablets can obviously improve the pathological state of the kidney in rats.Shenfukang tablet has a good therapeutic effect on membranous glomerulonephritis in rats.

目的:研究双去甲氧基姜黄素对硫代乙酰胺诱导的小鼠肝纤维化的保护作用及其机制.方法:将ICR小鼠随机分为正常对照组、模型组、水飞蓟素阳性对照组及双去甲氧基姜黄素高、中、低剂量组.除正常对照组外,其余各组均隔天1次连续7 w腹腔注射硫代乙酰胺溶液(200 mg/kg)诱导小鼠肝纤维化模型.双去甲氧基姜黄素高(200 mg/kg)、中(100 mg/kg)、低(50 mg/kg)剂量组1次/d,连续7w分别灌胃给予,正常对照组、模型组给予等体积相应溶剂.治疗结束后,采用生化分析法检测血清丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、总胆红素(IBI)及肝组织中羟脯氨酸(HYP)含量;酶联免疫吸附法(ELISA)检测血清透明质酸(HA)、层粘连蛋白(LN)、Ⅲ型前胶原(PC-Ⅲ)、Ⅳ型胶原(Ⅳ-C)水平;HE、Masson染色方法观察小鼠肝组织病理变化及肝纤维化的形成程度;蛋白免疫印迹法(Western blot)检测磷酸化的磷脂酰肌醇3-激酶(p-PI3K)、磷酸化的丝氨酸/苏氨酸蛋白激酶(p-Akt)、半胱氨酸天冬氨酸蛋白酶3(Caspase-3)、Bad蛋白的表达.结果:与模型组比较,双去甲氧基姜黄素各剂量组血清AST、ALT、IBI、HA、LN、PC-Ⅲ、Ⅳ-C和肝组织中HYP的水平显著降低(P＜0.05或P＜0.01),肝细胞变性坏死和纤维组织增生明显减轻,肝组织中p-PI3K、p-Akt、Caspase-3、Bad蛋白表达显著下调(P＜0.05或P＜0.01).结论:双去甲氧基姜黄素具有抗肝纤维化作用,其作用机制可能与PI3K/Akt信号通路有关.

The anti-allergic effect of berberine was evaluated in cellular and animal models of allergic responses. In this study, the results of the in vitro model of immunoglobulin (Ig) E-mediated mast cell degranulation showed that berberine significantly inhibited the release of β-hexosaminidase (β-HEX), histamine, IL-4 and TNF-α in rat basophilic leukemia cells (RBL-2H3 cells). Pretreatment with berberine prevented morphological changes in IgE-stimulated RBL-2H3 cells such as the recovery of an elongated shape. Pretreatment with berberine also suppressed the phosphorylation of antigen-induced Lyn, Syk, and Gab2, thus suppressing the downstream MAPK pathways. In the in vivo model of allergic responses, administration of berberine inhibited passive cutaneous anaphylaxis (PCA) in mice. The above results indicate berberine could suppress mast cell activation and allergic responses.

目的 探讨寄生壮骨颗粒对木瓜蛋白酶诱导大鼠骨关节炎的治疗作用 . 方法采用膝关节内注射10％木瓜蛋白酶和0.03mol/L L-半胱氨酸混合溶液制备大鼠骨关节炎模型,造模后分别给予寄生壮骨颗粒(8.69g/kg、4.35g/kg、2.12g/kg)及阳性药盐酸氨基葡萄糖(0.13g/kg),每日1次,连续灌胃给药4周.测定大鼠体重、膝关节肿胀度,血清中IL-1β、TNF-α、IL-6、MMP-3、MMP-13及滑膜组织中糖胺多糖的含量评价其治疗作用. 结果寄生壮骨颗粒高、中剂量组能够显著降低血清中IL-1β、TNF-α、IL-6、MMP-3、MMP-13的水平,增加滑膜组织中糖胺多糖的含量. 结论寄生壮骨颗粒对木瓜蛋白酶诱导大鼠骨关节炎具有治疗作用,其机制可能与降低血清中IL-1β、TNF-α、IL-6、MMP-3、MMP-13的水平和增加滑膜组织中糖胺多糖的含量有关.

目的 优选紫苏黑木耳乳制备工艺.方法 对紫苏黑木耳乳配方中黑木耳多糖与紫苏子油用量配比、多糖粉粒度以及助悬剂的用量进行了实验考察.结果 确定紫苏黑木耳乳制备工艺为:将蜂蜡加入到紫苏子油中,于60℃加热熔融,放冷备用.黑木耳提取多糖,粉碎成能过120目筛的细粉,加入到上述冷却的紫苏子油蜂蜡的混合液中,充分混匀,用胶体磨均质乳化.结论 紫苏黑木耳乳的制备工艺合理可行,可为紫苏黑木耳乳生产应用提供理论依据.

Coptisine is one of the main components of isoquinoline alkaloids in the coptidis rhizome. The effect of coptisine on allergic rhinitis has not been investigated. In this study, we report the effects and mechanisms of coptisine using monoclonal anti-2,4,6-dinitrophenyl-immunoglobulin (Ig) E/human serum albumin (DNP-IgE/HSA)-stimulated rat basophilic leukemia cells (RBL-2H3 cells) in vitro and an ovalbumin (OVA)-induced allergic rhinitis (AR) in mice. The results showed that coptisine markedly decreased the levels of β-hexosaminidase, histamine, interleukin (IL)-4, and tumor necrosis factor (TNF)-α. Coptisine also prevented morphological changes, such as restoring an elongated shape, inhibiting granule release on toluidine blue staining, and reorganizing inhibited filamentous actins (F-actin). Additionally, coptisine blocked the phosphorylation of phosphoinositide3-kinase (PI3K)/Akt (as known as protein kinase B(PKB)) in RBL-2H3 cell. Furthermore, the results showed that coptisine suppressed OVA-induced allergic rhinitis symptoms, such as nasal rubbing and OVA-specific IgE, and histamine, IL-4 and TNF-α levels in the serum of AR mice. These data suggested that coptisine should have inhibitory effects on the inflammatory responses of mast cells, and may be beneficial for the development of coptisine as a potential anti-allergic drug.

目的:探究旋覆花中黄酮对高血脂症模型大鼠的影响.方法:通过给予高脂饲料建立高血脂症模型,经口给予各剂量旋覆花总黄酮4周,测定大鼠日均进食量,动物处死前12 h分笼饲养,12 h后收集大鼠粪便,麻醉后腹主动脉取血,收集血清与肝脏,分别测定其血清中总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白-胆固醇(LDL-C)、高密度脂蛋白-胆固醇(HDL-C)、超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物还原酶(GSH-PX)、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6、白细胞介素(IL)-10水平,测定肝脏中总胆固醇含量、粪便中胆汁酸含量,肝组织石蜡切片苏木素-伊红(HE)常规染色.结果:连续给予高脂饲料8周后,相较于对照组,高血脂症模型大鼠的体质量、肝脏中胆固醇水平显著升高,血清中TC、TG、LDL-C水平显著升高,HDL-C水平显著降低,肝脏出现严重的脂肪变性,血清中GSH-PX和SOD水平显著降低,MDA水平显著升高,TNF-α与IL-6水平显著升高,IL-10水平显著降低.旋覆花总黄酮能够改善脂肪肝程度,降低高脂血症大鼠体质量、肝脏中胆固醇水平血清中TC、TG、LDL-C水平,升高HDL-C水平与粪便中胆汁酸水平;同时能够提高GSH-PX和SOD活性,降低MDA水平;降低TNF-α、IL-6水平,升高IL-10水平.结论:旋覆花总黄酮能够通过抑制脂质过氧化反应发挥促进胆汁酸排泄及抑制炎症的作用,进而发挥降血脂及改善脂肪肝作用.