To explore the molecular mechanism of Xuefu Zhuyu Decoction (XFZYD) against myocardial fibrosis. The active components of XFZYD were identified by high performance liquid chromatography (HPLC). Network pharmacology, molecular docking, and affinity dot-mass spectrometry (AD-MS) were used to predict and validate the binding interaction between XFZYD components and copper transporter 1 (CTR1). Sixty male Kunming mice were randomly divided into 6 groups using a random number table. Control, isoproterenol hydrochloride (ISO), captopril, low-, medium-, and high-dose XFZYD (5.69, 11.38, and 22.76 g/kg) groups, with 10 mice in each group. Except the control group, mice received daily subcutaneous injection of ISO (10 mg/kg) for 28 d to induce myocardial fibrosis, concurrently treated with respective drugs by gavage. Cardiac function was assessed by echocardiography (ECG) and electrocardiography (UCG). Serum myocardial injury markers and transforming growth factor beta 1 (TGF-β 1) were measured by a biochemical analyzer and enzyme-linked Immunosorbent assay (ELISA). Pathological changes and collagen deposition was observed using HE, Masson and sirius red staining methods. Copper content in cardiac tissue was determined by inductively coupled plasma mass spectrometry (ICP-MS), and protein expressions of collagen I, III, alpha-smooth muscle actin (α-SMA), lysyl oxidase (LOX), CTR1, copper chaperone for superoxide dismutase (CCS), and cytochrome c oxidase 17 (COX17) were detected by Western blot, immunohistochemistry, and immunofluorescence. In vitro, TGF-β 1 (5 ng/mL)-stimulated NIH-3T3 fibroblasts were treated with XFZYD (60 mg/L), with or without CuCl2 (20 µ mol/L) or SLC31A1 overexpression for 24 h, and the same indicators were evaluated. HPLC identified 7 major components in XFZYD. Network pharmacology revealed that XFZYD targets copper metabolism related genes. Molecular docking showed strong binding affinities between the 7 compounds and CTR1, and AD-MS confirmed direct binding of paeoniflorin and amygdalin to CTR1. In vivo, XFZYD could ameliorate the collagen deposition, cardiac dysfunction, and elevated levels of collagen I/III, α-SMA, LOX, and copper content exhibited in ISO-induced myocardial fibrosis mice (P<0.05 or P<0.01). In vitro, XFZYD had the effects of suppressing copper overload and the upregulation of LOX, collagen I/III, and α-SMA in TGF β 1 stimulated NIH-3T3 fibroblasts, whereas co-treatment with CuCl2 exacerbates these fibrotic responses and attenuates the protective effect of XFZYD (P<0.05 or P<0.01). XFZYD had the effect of partially reversing the enhanced copper accumulation, LOX activation, and collagen deposition induced by SLC31A1 (CTR1) overexpression in TGF β 1 stimulated fibroblasts, and SLC31A1 overexpression reduces its efficacy (P<0.05 or P<0.01). XFZYD exerted a protective effect against ISO-induced myocardial fibrosis. The mechanism may be related to regulating the CTR1–copper–LOX axis, thereby reducing excessive collagen deposition and cross-linking in cardiac fibroblasts.

Acute myocardial infarction (AMI) is a leading cause of heart failure, often accompanied by myocardial fibrosis (MF), characterized by excessive extracellular matrix accumulation. Endothelial-to-mesenchymal transition (EndMT) plays a key role in MF progression post-AMI. Neuregulin-1 (NRG-1), a growth factor with cardioprotective properties, has emerged as a potential therapeutic target. Tongxinluo (TXL), a traditional Chinese medicine, mitigates MF by upregulating NRG-1. This study elucidates the mechanisms underlying the protective effects of NRG-1 and TXL against MF following AMI. Left anterior descending artery ligation established a model for mice with AMI. Adeno-associated virus was used to modulate NRG-1 expression in the myocardium. Echocardiography assessed cardiac function, and histological staining was used to evaluate MF. Expression levels of markers for myofibroblasts (α-SMA, FSP-1) and endothelial cells (CD31, VE-cadherin) were analysed to investigate EndMT. The involvement of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signalling pathway in NRG-1’s protective mechanism was validated using biochemical methods. Tongxinluo was administered to mice with AMI via gavage for 4 weeks, and its effects on cardiac function, MF and EndMT were assessed. Overexpression of NRG-1 in mice with AMI ameliorated cardiac dysfunction and reduced interstitial and perivascular fibrosis, whereas NRG-1 deficiency exacerbated these effects. NRG-1 protected against EndMT, as evidenced by changes in myofibroblast and endothelial cell markers. The PI3K/AKT signalling pathway was involved in NRG-1’s protective mechanism against MF. The administration of TXL to mice with AMI improved cardiac function and reduced MF by activating NRG-1. Furthermore, TXL inhibited EndMT post-AMI through the NRG-1/PI3K/AKT pathway. NRG-1 and TXL protect against MF post-AMI by mitigating EndMT through the PI3K/AKT pathway. These findings suggest that targeting NRG-1 or using TXL may be promising therapeutic strategies for MF following AMI.

目的 探索通补防颤方对乙酰胆碱-氯化钙(Ach-CaCl2)诱导大鼠阵发性房颤(paroxysmal atrial fibrillation,PAF)的防治作用.方法 将雄性SD大鼠随机分为空白对照组、模型组、通补防颤方低、中、高剂量组、胺碘酮组.采用尾静脉注射Ach-CaCl2混合液建立PAF大鼠模型.通过心电图检测大鼠房颤易感性,电Mapping检测大鼠心房传导离散度,小动物超声仪检测大鼠左心房直径及左心房面积,Masson染色观察大鼠心房肌组织纤维情况,免疫组化和Western blot法检测大鼠酪氨酸羟化酶(tyrosine hydroxylase,TH)蛋白表达.结果 Ach-CaCl2尾静脉注射7 d后大鼠心电图表现为P波消失,代之以不规则的f波,RR间期绝对不规则;与模型组相比,通补防颤方低、中、高剂量组及胺碘酮组不同程度延长大鼠房颤诱发时间,缩短房颤持续时间;降低心房传导离散度;缩小左心房直径及左心房面积;改善心房肌组织排列,减少纤维沉积;降低TH蛋白平均分布密度及分布不均一程度;下调TH蛋白表达水平.结论 通补防颤方可降低Ach-CaCl2诱导PAF大鼠的房颤易感性、心房传导离散度,改善电重构、结构重构及神经重构,为通补防颤方在防治PAF的临床应用提供数据支撑,以期提高PAF的临床治疗水平.

纤维化是各组织器官在受到损伤刺激后启动的修复反应,是机体的一种自我保护机制.研究发现,内皮间质转分化(endothelial-to-mesenchymal transition,EndMT)参与心脏、肺脏、肾脏、肝脏、胰腺等多种器官纤维化的生理病理过程,已成为纤维化疾病研究的一个重点.该文将总结EndMT的调控机制及其在器官纤维化中作用,以及以EndMT为靶点的相关治疗进展,以期为器官纤维化的防治提供新的靶点.

Background: Atherosclerosis (AS) is a common comorbidity of chronic obstructive pulmonary disease (COPD) and the main cause of death in patients with COPD. Systemic inflammation is a significant mechanism of COPD with AS. The dysfunction of pulmonary microvascular barrier is involved in the formation of chronic inflammation in COPD, and its functional disruption will induce systemic inflammation. Atorvastatin (Ato) is a common medicine for the treatment of AS; however, the effect is not ideal for COPD combined with AS. Tongxinluo (TXL) improves the function of vascular endothelial cells. This study aims to prove that the impairment of pulmonary microvascular barrier function participated in the process of COPD aggravating AS and investigated whether TXL enhances the therapeutic effect of Ato on COPD with AS by protecting the pulmonary microvascular endothelial barrier function. Methods: In vivo, the COPD with AS model of ApoE-/- mice was established by cigarette smoke combined with a high-fat diet. The animals were administered TXL (1.5 g/kg/day), Ato (10 mg/kg/day), and TXL+Ato once a day for 20 weeks. Then, lung function, lung microvascular permeability, lung inflammation, systemic inflammation, serum lipid level, atheromatous plaque formation, and the biomarker of endothelial damage were measured. In vitro, human pulmonary microvascular endothelial cells (HPMECs) were pretreated with TXL for 6 h and incubated with cigarette smoke extract (CSE) for 24 h to establish a model of CSE-induced pulmonary microvascular barrier dysfunction. The permeability of the endothelial monolayer, inflammatory cytokines, endothelial damage biomarkers, tight junction proteins were determined. Results: Cigarette smoking significantly exacerbated, which induced by high fat diet, the pulmonary function decline, pulmonary microvascular endothelial barrier dysfunction, pulmonary and systemic inflammation, and atherosclerotic plaque. These changes were reversed by TXL-Ato combination; the combination therapeutic effect was better than that of Ato alone. In addition, TXL protected the function of HPMEC barrier and inhibited the inflammation in CSE-induced HPMECs. Conclusions: COPD aggravates AS, the mechanism may be the destruction of pulmonary microvascular barrier function and thus lung inflammation triggers systemic inflammation. In treating COPD with AS, TXL enhances the anti-AS effect of Ato protecting the pulmonary microvascular barrier.

慢性阻塞性肺疾病(COPD)是一个严重的全球性健康问题,通常与心血管疾病(CVD)合并发生.它们之间有许多共同的危险因素,但2个疾病之间相互影响的机制尚不明确,且在治疗方面目前的指南主要限于单个疾病的治疗,缺乏合并症的管理方案.文章就COPD与CVD之间的共同发病因素、发病机制以及治疗策略方面进行综述.

Cardiovascular comorbidities are pervasive in chronic obstructive pulmonary disease (COPD) and often result in serious adverse cardiovascular events. Tongxinluo (TXL) has been clinically verified to treat atherosclerosis (AS), improve lung function and alleviate dyspnoea. The present study aimed to explore the effect of lung microvascular barrier dysfunction on AS in COPD and the potential pulmonary protective mechanisms of TXL in COPD complicated with AS. COPD complicated with AS was induced in mice by cigarette smoke (CS) exposure and high-fat diet (HFD) feeding. The mice were treated with atorvastatin (ATO), TXL or combination therapy (ATO+TXL) for 20 weeks. Pulmonary function, lung pathology, serum lipid levels, atherosclerotic plaque area and indicators of barrier function, oxidative stress and ferroptosis in lung tissue were evaluated. In vitro, human pulmonary microvascular endothelial cells (HPMECs) were pretreated with TXL for 4 h and then incubated with cigarette smoke extract (CSE) and homocysteine (Hcy) for 36 h to induce barrier dysfunction. Then the indicators of barrier function, oxidative stress and ferroptosis were measured. The results demonstrate that CS aggravated dyslipidaemia, atherosclerotic plaque formation, pulmonary function decline, pathological injury, barrier dysfunction, oxidative stress and ferroptosis in the HFD-fed mice. However, these abnormalities were partially reversed by ATO and TXL. Similar results were observed in vitro. In conclusion, pulmonary microvascular barrier dysfunction plays an important role by which COPD affects the progression of AS, and ferroptosis may be involved. Moreover, TXL delays the progression of AS and reduces cardiovascular events by protecting the pulmonary microvascular barrier and inhibiting ferroptosis.

阻塞性睡眠呼吸暂停综合征(OSAS)是一种常见的以睡眠时上气道反复塌陷为特征的慢性睡眠呼吸疾病,与高脂血症、动脉粥样硬化和心血管风险相关.近年来,已有研究证实OSAS是动脉粥样硬化(AS)形成的独立危险因素,会加速AS的发生和发展.目前有理论提出动脉粥样硬化发生的关键因素之一是动脉壁氧供需不平衡,而OSAS的典型特征是慢性间歇性缺氧(CIH),所以推测CIH可能是OSAS加速AS形成的中间机制,然而其具体机制尚未完全明确,因此现就其可能的机制进行综述,以期为临床治疗和研究提供启示.

OBJECTIVE: Cardiovascular disease (CVD) is a com mon comorbidity and a major cause of death in patients with chronic obstructive pulmonary disease (COPD). Pulmonary microvascular barrier dysfunction is in-volved in the development of chronic inflammation in COPD and induces systemic inflammation. Tongxinluo (TXL) improves the function of vascular endothelial cells. However, the effect of TXL on pulmonary micro- vascular barrier function remains unknown. This study aims to explore the molecular mechanism of pulmonary microvascular barrier dysfunction in COPD combined with atherosclerosis and the related targets of TXL in this dysfunction. STUDY DESIGN: In vivo, the COPD with atheroscle rosis mouse model on the ApoE(-/-) background was established by cigarette smoke combined with a high-fat diet. The animals were administered TXL, atorvastatin (Ato), and TXL+Ato once a day for 20 weeks. Then, the biomarkers of the Rac1/Cdc42 pathway were measured. In vitro, human pulmonary microvascular endothelial cells (HPMECs) were pretreated with TXL and incubated with cigarette smoke extract (CSE) to establish the model. The permeability of the endothelial monolayer and tight junction protein expression were determined. RESULTS: The Rac1/Cdc42 signaling pathway participated in the deterioration of the pulmonary microvascular barrier, and treatment with TXL decreased the levels of Rac1, Cdc42, and p-Rac1 + Cdc42. Then, knocking down the expression of Rac1 in HPMECs using small-interfering RNA decreased the protein levels of Rac1, Cdc42, and p-Rac1 +Cdc42 while increasing the ability of HPMECs to maintain the pulmonary micro- vascular barrier function, and TXL had a synergistic effect on the inhibition of the Rac1/Cdc42 signaling pathway with siRNA. CONCLUSION: The Rac1/Cdc42 pathway is involved in pulmonary microvascular barrier dysfunction, and TXL can protect pulmonary microvascular barrier function by inhibiting the expression of Rac1/Cdc42 signaling pathway-related proteins in HPMECs.

目的 观察解毒护肝方对药物性肝损伤大鼠TLR3/TNF-α/JNK2信号通路的影响.方法 采用对乙酰氨基酚灌胃制作大鼠肝损伤模型.将实验大鼠按体质量随机分为正常组、模型组、阳性对照组和解毒护肝方高、中、低剂量组,各给药组给予相应药液灌胃,正常组和模型组给予生理盐水灌胃.生化分析仪检测血清AST、ALT活性和总胆红素(TBIL)、直接胆红素(DBIL)含量;RT-PCR和Western blot分别检测肝组织JNK2基因和蛋白的表达;酶标仪检测肝组织匀浆肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)含量;免疫组化染色观察Toll样受体3(TLR3)蛋白表达.结果 与正常组比较,模型组大鼠ALT、AST、DBIL、TNF-α水平显著升高(P<0.01),JNK2 mRNA和p-JNK2、TLR3蛋白表达显著升高(P<0.01);与模型组比较,解毒护肝方中、低剂量组大鼠AST、ALT活性显著降低(P<0.05,P<0.01),解毒护肝方低剂量组大鼠DBIL含量显著降低(P<0.05),解毒护肝方高剂量组大鼠TNF-α 含量显著降低(P<0.01),解毒护肝方高、中剂量组大鼠JNK mRNA和TLR3蛋白表达均显著下调(P<0.05,P<0.01),p-JNK2蛋白表达有降低趋势,但差异无统计学意义(P>0.05).结论 解毒护肝方对药物性肝损伤大鼠有明显的保护作用,以中、低剂量组效果最为明显,其机制可能与调控TLR3/TNF-α/JNK2信号通路有关.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">目的观察泽泻汤加味方对高脂血症大鼠血脂及结肠组织水通道蛋白3和4（AQP3、AQP4）基因、蛋白表达的影响。方法将60只雄性SD大鼠随机分为对照组、模型组、阳性对照组（辛伐他汀）及泽泻汤加味方高、中、低剂量组,采用喂饲高脂饲料方法复制大鼠模型,造模同时给予相应药物干预,连续5周;观察大鼠血清中甘油三酯（TG）、胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）含量变化,运用RT-PCR、Western blot方法检测大鼠结肠组织中AQP3和AQP4基因、蛋白表达情况。结果与对照组比较,模型组大鼠血清中TG、TC、LDL-C含量[分别为（2.183±0.204）、（2.013±0.250）、（1.267±0.087）mmol/L]升高,HDL-C含量[（0.731±0.085）mmol/L]降低（P &lt;0.05）;与模型组比较,高剂量泽泻汤加味方组大鼠血清中TG、TC、LDL-C含量[分别为（1.205±0.139）、（1.164±0.197）、（0.787±0.057）mmol/L]下降,HDL-C含量[（0.904±0.115）mmol/L]升高（P &lt;0.05）。与对照组比较,模型组大鼠结肠组织中AQP3和AQP4蛋白表达水平[分别为（0.944±0.052）、（0.701±0.067）]升高（P &lt;0.01）;与模型组比较,高剂量泽泻汤加味方组大鼠结肠组织中AQP3和AQP4蛋白表达水平[（0.502±0.085）、（0.366±0.061）]均降低,呈剂量效应关系（P &lt;0.05）。结论泽泻汤加味方具有调节血脂作用,其机制可能与结肠组织AQP3和AQP4蛋白表达调控有关。</span>

以中医脉络学说为指导,基于脉络与现代医学中小血管、微血管、微循环的同一性,提出"脉络-血管系统病"这一新概念,心肌梗死再灌注后的微血管功能障碍导致心肌纤维化,归属于这一病理范畴.基于"脉络-血管系统病"探析心肌梗死心肌纤维化的病机,并应用脉络学说核心理论——"营卫理论"为通络治疗提供理论指导.

目的 通过观察泽泻汤加味方对高脂血症大鼠胃黏膜水通道蛋白(AQP)4蛋白表达的影响.方法 将60只健康SD大鼠随机分为空白组、模型组、辛伐他汀对照组和泽泻汤加味方高、中、低剂量组,每组10只,造模的同时给予相应药物治疗.第5周末检测血清中三酰甘油(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)的含量,观察肝组织形态学变化,并运用免疫组化及Western印迹法检测大鼠胃黏膜中AQP4蛋白的表达变化.结果 模型组TG、TC、LDL-C含量显著升高、胃黏膜AQP4表达显著增强(P<0.01),HDL-C含量显著降低(P<0.01或P<0.05),各用药组大鼠血清中TG、TC、LDL-C含量显著降低、胃黏膜AQP4的表达显著减弱,HDL-C含量显著升高(P<0.01或P<0.05).结论 泽泻汤加味方具有良好的调节血脂作用,可能是通过下调胃黏膜AQP4蛋白的表达调节水液代谢,抑制水湿停聚,祛除痰浊.

Objective:to study the effect of supplemented formula of Alisma decoction on Aquaporin-3(AQP3) expression in gas-tric mucosa of hyperlipidemia rats,and to explore the mechanism of prevention and treatment of hyperlipidemia. Methods:60 healthy SD rats were randomly divided into blank group, model group, Simvastatin control group (short for control group), and high dose, middle and low dose group of Alisma decoction. At the end of the fifth week,triglyceride(TG),total cholesterol(TC),high density lipoprotein (HDL-C),low density lipoprotein (LDL-C) levels and liver histological changes in rat serum were observed and the ex-pression of AQP3 protein was detected in rat gastric mucosa by immunohistochemistry and Western Blot method. Results: TG, TC, LDL-C levels of model group increased and AQP3 expression of gastric mucosa was enhanced( P <0.01),the content of HDL-C de-creased( P < 0.01 or P < 0.05);of the medication groups, TG, TC, LDL-C levels decreased, AQP3 expression decreased, and HDL-C increased( P < 0.01 or P < 0.05).Conclusion:Supplemented formula of Alisma decoction has the effect of regulating blood lipid. It may be one of the mechanisms of preventing and treating hyperlipidemia by reducing the expression of AQP3 in gastric muco-sa,regulating the metabolism of water and eliminating the pathological factors of phlegm turbidity.

OBJECTIVE: To observe the effects of Modified Rhizoma Alismatis decoction on the expression of aquaporin 8 (AQP8) in liver tissue of hyperlipemia model rats, and to investigate the mechanism of preventing and treating hyperlipemia.METHODS: Total of 60 rats were randomly divided into blank control group (distilled water), model group, positive control group (simvastatin 1. 89 mg/kg) and modified Rhizoma Alismatis decoction high-dose, medium-dose and low-dose groups (29. 56, 14. 78, 7. 39 g/kg, calculated by crude drug), with 10 rats in each group. Those groups were given high-fat diet to induce hyperlipemia model and given relevant medicine intragastrically once a day for consecutive 5 weeks except that blank control group was given normal diet. After administration, the serum contents of TG, TC, HDL-C and LDL-C in rats were detected, and the pathomorphology changes of liver tissue were observed; the mRNA and protein expression of AQP8 in liver tissue were detected. RESULTS: Compared blank control group, the serum contents of TG, TC and LDL-C in model group were increased significantly (P<0. 05 or P<0. 01),while the serum content of HDL-C was decreased significantly (P<0. 01); pathological changes were found in liver tissue, such as irregular cell arrangement and hepatic sinusoidal hyperemia and edema; mRNA and protein expression of AQP8 in liver tissue were increased significantly (P<0. 01). Compared with model group, above indexes of treatment groups were improved significantly (P<0. 05 or P<0. 01); the structure of liver tissue tended to be normal and the fatty degeneration was obviously alleviated. CONCLUSIONS: Modified Rhizoma Alismatis decoction can regulate the mRNA and protein expression of AQP8 in liver tissue so as to play the effects on the prevention and treatment of hyperlipidemia.

目的:通过研究泽泻汤加味方对高脂血癌大鼠肝细胞水甘油通道蛋白9(AQP9)表达的影响,探讨其防治高脂血症的作用机制.方法:将60只健康雄性SD大鼠随机分为正常组、模型组、辛伐他汀1.89mg/kg组和泽泻汤加味方7.39、14.78、29.56g/kg组,采用喂饲高脂饲料的方法复制高脂血症模型,造模的同时给予相应药物治疗.治疗5周后检测大鼠血清中TG、TC、HDL-C、LDL-C的含量、观察肝组织形态学变化,并运用RT-PCR及Western Blot法检测肝细胞AQP9基因、蛋白的表达变化.结果:模型组大鼠血清中TG、TC、LDL-C的含量及肝细胞中AQP9表达升高,HDL-C含量显著降低,肝组织出现脂肪变性;泽泻汤加味方29.56g/kg、14.78g/kg、7.39g/kg组和辛伐他汀1.89mg/kg组大鼠血脂中TG、TC、LDL-C的含量及肝细胞AQP9的表达均显著降低,HDL-C含量显著升高,肝组织的形态结构亦趋于正常.结论:泽泻汤加味方具有较好的调节血脂作用,推测该方通过下调肝细胞AQP9的表达、抑制甘油的渗透、减少TG的合成,是防治高脂血症的作用机制之一.

张一昕教授在慢性肝病诊治中,以疏肝健脾、 消痰化瘀、 祛湿通滞立法,灵活运用组药,常以泽泻、白术、 路路通健脾祛湿、 化浊通络,以三七、 阿胶、 桔梗、 牛膝理血逐瘀、 升降同调,以茵陈、 八月札、 六月雪退黄疏肝、 引邪外出,以半枝莲、 山慈菇、 枸杞子直捣热毒、 兼顾气阴,以土鳖虫、 山甲珠、 钩藤软坚散结、 破癥消积,临床疗效颇佳.

Objective:To study the influence on the rats liver factor and the mRNA,protein expression of cytochrome P450 2El (CYP2E1),cytochrome P450 3A4(CYP3A4) by combined use of vinegar-preparing kansui and Radix Glycyrrhizae Preparata.Methods:Sixty male Wistar rats,weighted 140 ～ 160 g,were randomly assigned to normal group,vinegar-preparing kansui group,Radix Glycyrrhizae Preparata group,compatibilities of vinegar-preparing kansui and Radix Glycyrrhizae Preparata group,Gansui Banxia Decoction group,12 rats in each group.The normal group received saline irrigation and the remaining groups were given the corresponding liquid orally,administration volume 1 mL/100 g,continuous administration for 14 days.Weigh every 7 days.Freely eat food and water.14 days after the anesthesia with 3.5％ hydrate of chlorine (1 mL/100 g),the levels of serum alanine transaminase (ALT),aspartate transaminase (AST),lactate dehydrogenase(LDH) were detected by Automatic Biochemistry Analyzer.The liver tissues in the formalin-fixed were studied by light microscopy.The mRNA expression levels of CYP2E1 and CYP3A4 in rats liver microsomes were determined by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).The protein expression levels of CYP2E1 and CYP3A4 were detected by Western blotting.The experimental data was processed by SPSS 11.5 software and the measurement data was compared by using analysis of variance.The homogeneity of variance used LSD and homogeneity of variance used Dunnett T3.The count data used non parametric test and the significant difference was at P ＜ 0.05.Results:There was no significant difference among every groups for ALT.Compared with normal group,administration groups with vinegar-preparing kansui could decrease plasma AST level which was decreased significantly in Gansui Banxia Decoction group.LDH levels of each drug administration group were lowered significantly than that of the normal group.The expression levels of mRNA and protein of CYP2E1 were significantly increased in co-administration group.The expression levels of mRNA and protein of CYP3A4 were significantly decreased in co-administration group.But,Gansui Banxia Decoction group could decrease the level of CYP2E1,with increasing the level of CYP3A4.Conclusion:This experiment from the molecular mechanism of the compatibility of vinegar-preparing kansui and Radix Glycyrrhizae Preparata increased toxic effects,while this compound can reduce the toxicity.However,it was found that the combined medication of vinegar-preparing kansui and Radix Glycyrrhizae Preparata did not affect the mu tual toxicity remarkably in biochemical index.Many other mechanisms need to be further studied because drug interaction is complex.

To discuss the mechanism of modified Rhizoma Alismatis Decoction on prevention and treatment of hyperlipemia,through investigating hepatic expressions of AQP3 in rats with hyperlipemia.60 Male Sprague-Dawley rats were randomly divided into 6 groups:Control group,Model control group,Simvastatin control group,High-dose of modified Rhizoma Alismatis Decoction group,Middle-dose of modified Rhizoma Alismatis Decoction group,Low-dose of modified Rhizoma Alismatis Decoction group.Rats in control group were fed with ordinary forage,and the others were fed with high-fat forage.At the same time,each treatment group was administrated with appropriate drug.Then TC,TG,HDL-C and LDL-C of serum were detected,the genetic expression of AQP3 in colon tissue were detected with RT-PCR and the protein expression of AQP3 in colon tissue were detected with immunohistochemical means and Western Blot after 5 weeks.In the model control group,the content of TG,TC,LDL-C in serum and the expression of AQP3 in colon tissue were significantly elevated,while the content of HDL-C was significantly reduced.After treatment,the contents of TG,TC,LDL-C and the expression of AQP3 in every treatment groups were reduced,while the contents of HDL-C were elevated.Modified Rhizoma Alismatis decoction had a satisfying effect on regulating the blood lipid.Increasing the genetic and protein expression of AQP3 in colon tissue,regulating the water fluid metabolism,preventing the formation of sputum and removing the pathogenic factors could be viewed as mechanisms of modified Rhizoma Alismatis Decoction concerning prevention and treatment of hyperlipemia.

Objective:To primarily discuss the mechanism of Rhizoma Alismatis Decoction on prevention and treatment of hyperlipemia through investigating hepatic expressions of LXRα and ABCA1 mRNA in rats with hyperlipemia.Methods:The rats' model of hyperlipemia was duplicated by high-fat diet feeding.High and low dose of Rhizoma Alismatis Decoction,as well as Xuezhikang Capsule,was administrated in respectively designed groups,and corresponding indexes were detected 4 weeks later.Results:Rhizoma Alismatis Decoction could significantly reduce serum concentrations of TC,TG and LDL (P ＜0.01),while increasing the concentration of HDL (P ＜ 0.01) and strengthening the expressions of LXRα and ABCA1mRNA (P ＜ 0.01).Conclusion:Strengthening expressions of LXRα /ABCA1 could be viewed as mechanisms of Rhizoma Alismatis Decoction on prevention and treatment of hyperlipemia.