Barrett食管(BE)是食管腺癌前期病变,其病程迁延难愈,临床表现复杂多样且不典型.魏睦新教授认为,BE病位在食管,属胃所主,与肝、脾关系密切,并以辛开苦降为法,佐以理气、化痰、消瘀治标,以半夏泻心汤合左金丸化裁,自创辛开苦降散结方治疗,临床取得良好疗效.

目的 研究猪苓多糖抑制胃黏膜上皮细胞(GES-1)间充质转化的作用和机制.方法 应用N-甲基-N'-硝基-N-亚硝基(MNNG,40μmol·L-1)诱导GES-1细胞间充质转化模型,造模同时给予猪苓多糖(1.25、2.50、5.00、10.00 mg·mL-1)处理24、48 h后,CCK-8法检测细胞增殖能力;造模同时给予猪苓多糖(5.00 mg·mL-1)处理48 h后,实时定量PCR(qRT-PCR)法检测猪苓多糖对 N-cadherin、Snail、Twist、Fibronection 及 Vmention mRNA表达的影响;Western blotting法检测 E-cadherin、N-cadherin、Snail、Twist、Fibronetin、Vimentin、STAT3、p-STAT3、JAK2、p-JAK2 蛋白表达.裸鼠分别 sc经 MNNG 40 μmol·L-1 处理48 h后的 GES-1 细胞(5 × 107·mL-1,0.2 mL)、胃癌细胞 SGC7901(5× 107·mL-1,0.2 mL,阳性对照),1个月后观察各组成瘤及体质量情况,注射局部进行HE染色后行组织病理学观察,验证GES-1细胞经MNNG处理后是否达到肿瘤阶段.结果 与模型组比较,随猪苓多糖浓度的增加,GES-1细胞增殖能力逐渐上升,到达5mg·mL-1时增殖能力最高,差异显著(P＜0.01、0.001);猪苓多糖组N-cadherin、Snail、Twist、Fironetion 及 Vimentin 的 mRNA表达均显著下降(P＜0.05、0.01、0.001);猪苓多糖组 E-cadherin 蛋白表达显著上升(P＜0.05),N-cadherin、Snail、Twist、Fibronetion、Vimentin 及通路蛋白STAT3、p-STAT3、JAK2、p-JAK2表达显著下降(P＜0.05、0.01、0.001).对照组和MNNG处理的GES-1 组未见瘤体形成,阳性对照SGC7901组注射后1周左右局部出现瘤体,1个月瘤体长至6 cm左右;MNNG处理的GES-1组裸鼠精神较差,体质量明显减轻,SGC7901组裸鼠状态差,体质量大幅减轻;对照组和MNNG组病理染色显示为正常的皮肤组织,阳性对照组显示为肿瘤组织.结论 猪苓多糖可能通过抑制JAK2-STAT3通路干预MNNG诱导的GES-1细胞上皮间充质化.

Hypoxemia is 1 of the most common complications in the patients with acute Type A aortic dissection (ATAAD). This study aimed to summarize the risk factors, management strategies and long-term prognosis for postoperative hypoxemia in ATAAD patients. Baseline characteristics and clinical data of all the patients were collected. Patients were divided into 2 groups according to the PaO2/FiO2 after surgery: Hypoxemia group (n = 142) and Non-hypoxemia group (n = 68). The differences in gender, age, body mass index, operation time, cardiopulmonary bypass (CPB) time, aortic cross-clamping time, deep hypothermic circulatory arrest time, preoperative PaO2/FiO2, postoperative PaO2/FiO2, PaO2/FiO2 before extubating, time of mechanical ventilation, length of intensive care unit stay, length of hospital stay, in-hospital mortality, and overall mortality were compared between the 2 groups. The incidence of postoperative hypoxemia in this study was 67.6% (142/210). body mass index (26.4 ± 3.8 vs 24.4 ± 3.3kg/m2, P < .001) in the hypoxemia group were markedly higher and CPB time (196.3 ± 41.0 vs 181.0 ± 37.3 minutes, P = .010) in the hypoxemia group were significantly longer than those in the non-hypoxemia group. While preoperative PaO2/FiO2 (229.7 ± 91.4 vs 299.7 ± 101.2mmHg, P < .001) was significantly lower than those in the non-hypoxemia group. In the hypoxemia group, PaO2/FiO2 before extubating was significantly higher than that after operation, and the difference was significant. Logistic regression analysis showed that overweight (odds ratio [OR]: 1.113, P = .030), CPB time (OR: 1.009, P = .043) and preoperative PaO2/FiO2 (OR: 0.994, P = .001) were independent risk factors for postoperative hypoxemia. Further follow-up results showed no significant difference in long-term mortality between the 2 groups. Logistic regression analysis revealed that PaO2/FiO2 before extubating (OR: 0.985, P < .001), paraplegia (OR: 10.994, P = .019), acute renal failure (OR: 12.590, P < .001), re-operation (OR: 4.721, P = .014) and re-admission to intensive care unit (OR: 13.727, P = .001) were independent risk factors for long-term mortality. Our results showed that overweight and prolonged CPB time were risk factors for postoperative hypoxemia in ATAAD patients. While PaO2/FiO2 before extubating were independent risk factors for long-term mortality, indicating that active correction of hypoxemia and maintain a higher PaO2/FiO2 before extubating may help to improve the prognosis of the ATAAD patients.

Background: This study aimed to examine the effect of sodium butyrate on severe acute pancreatitis-related gut barrier injury in a rat model and explore its mechanism. Methods: Male rats randomly fell into 3 groups, that is, the control, the severe acute pancreatitis group, and the severe acute pancreatitis + butyrate group. Rats in the control group received sham operation, while rats in the severe acute pancreatitis group and severe acute pancreatitis + butyrate group received severe acute pancreatitis induction by intraductal infusion of 4% sodium taurocholate. After that, rats in the severe acute pancreatitis + butyrate group were fed with sodium butyrate solution with free access. Intestinal barrier injury was measured based on the expression of tight junction proteins by reverse transcription polymerase chain reaction, Western blotting assay as well as immunohistochemical staining. The variation of Treg cells was measured by reverse transcription polymerase chain reaction, Western blotting assay, immunohistochemical staining, and flow cytometry analysis. Results: Compared to rats in the control, rats in the severe acute pancreatitis group showed significantly higher pathohistological scores (P <.001) in the intestine, as well as decreased expression of occludin and ZO-1. While, rats in the severe acute pancreatitis + butyrate group showed mitigated histologic lesions (P <.05) and increased expressions of occludin and ZO-1. In addition, rats in the severe acute pancreatitis group showed the obvious reduction in the expressions of Foxp3 and GPR109a and the decreased percentage of Treg cells in the intestine (P <.001) compared to rats in the control. However, rats in the severe acute pancreatitis + butyrate group showed markedly increased expressions of Foxp3 and GPR109a and the upregulated percentage of Treg cells (P <.01). Conclusion: Butyrate could significantly mitigate the intestinal injury induced by severe acute pancreatitis, probably by inducing the differentiation of Treg cells.

目的 观察解郁化痰消瘀方治疗胃癌前病变(肝胃不和型)患者的疗效,探讨其治疗特色及优势.方法 将80例患者随机分为治疗组40例和对照组40例.治疗组采用解郁化痰消瘀方治疗,对照组采用摩罗丹治疗,2组疗程均为6个月.比较2组患者治疗前和治疗6个月后中医证候积分、胃镜下黏膜病理积分、汉密尔顿焦虑量表(HAMA)和汉密尔顿抑郁量表(HAMD)评分,并综合比较2组患者的疗效.结果 治疗6个月后,2组患者胃脘或胁肋胀满、嗳气反酸、胸闷、饮食减少等证候积分均下降,治疗组上述证候积分及总积分优于对照组,差异有统计学意义(P＜0.05).治疗6个月后,2组患者内镜下胃黏膜萎缩、肠化及异型增生积分低于治疗前,且治疗组胃黏膜萎缩、肠化积分低于对照组,差异有统计学意义(P＜0.05).治疗6个月后,治疗组患者HAMA和HAMD评分分别为(9.33±2.08)、(8.38±2.13)分,低于治疗前的(17.58±3.36)、(13.33±3.40)分,对照组治疗后HAMA评分为(14.43 ± 2.71)分,低于治疗前的(17.03±4.05)分,差异有统计学意义(P＜0.05).治疗6个月后,治疗组HAMA及HAMD评分均低于对照组,差异有统计学意义(P＜0.05).治疗组总有效率为95.00％(38/40),高于对照组的77.50％(31/40),差异有统计学意义(P＜0.05).结论 解郁化痰消瘀方可有效改善胃癌前病变(肝胃不和型)患者胃黏膜病理改变,同时改善患者焦虑和抑郁状态.

1 化痰消瘀汤 组 成:陈皮10 g,法半夏10 g,茯苓15 g,丹参15 g,生蒲黄10 g(包煎),白花蛇舌草15 g,仙鹤草15 g,吴茱萸3 g,黄连3 g,海螵蛸20 g,炙甘草3 g. 功 效:化痰消瘀,和胃解毒. 主 治:胃癌前期病变(痰瘀互结证). 用 法:每日1剂,水煎,分2次服. 方 解:方中陈皮燥湿化痰、理气和胃,丹参活血化瘀、祛瘀生新,共为君药;法半夏和胃祛湿化痰,且能散结,茯苓健脾利水渗湿,生蒲黄活血化瘀止痛,共为臣药;白花蛇舌草、仙鹤草清热化瘀抗癌,黄连、吴茱萸、海螵蛸调和肝胃以止酸,皆为佐药;炙甘草调和诸药.诸药合用,共奏化痰消瘀、和胃解毒之功.

目的:探讨急危重症患者中正常甲状腺病态综合征（ESS）与凝血功能的相关性。方法:纳入130例ICU的急危重症患者，根据是否存在ESS分为ESS组（92例）和非ESS组（38例），检测两组患者的凝血功能指标[凝血酶原时间（PT）、活化部分凝血酶原时间（APTT）、纤维蛋白原（FIB）、血浆凝血酶时间（TT）、D-二聚体（D-D）、血小板计数（PLT）、平均血小板容积（MPV）、血小板分布宽度（PDW）]，白蛋白，炎症相关指标[白细胞计数（LC）及降钙素原（PCT）]及甲状腺功能指标[三碘甲状腺原氨酸（TT3）、甲状腺素（TT4）、游离三碘甲状腺原氨酸（FT3）、游离甲状腺素（FT4）及促甲状腺激素（TSH）]，并采用Spearman相关分析对甲状腺功能指标与凝血功能指标之间的相关性进行分析。结果:与非ESS组比较，ESS组患者的PT[12（11，13）s vs. 13（12，16）s，Z = 3.080，P = 0.002]、APTT[28（25，31）s vs. 33（29，39）s，Z = 4.408，P < 0.001]均显著延长，D-D[2.1（1.0，4.7）mg/L vs. 4.8（2.3，7.1）mg/L，Z = 3.301，P = 0.001]及PCT[0.17（0.03，0.41）μg/L vs. 1.10（0.29，9.84）μg/L，Z = 4.220，P < 0.001]水平均显著升高，白蛋白[36（32，37）g/L vs. 32（28，34）g/L，Z = 3.604，P < 0.001]、TT3[1.3（1.1，1.4）nmol/L vs. 0.6（0.6，0.7）nmol/L，Z = 8.462，P < 0.001]、TT4[95（82，111）nmol/L vs. 56（40，72）nmol/L，Z = 6.816，P < 0.001]、FT3[4.0（3.5，4.4）pmol/L vs. 2.3（1.7，2.6）pmol/L，Z = 8.622，P < 0.001]、FT4[（13.2 ± 1.9）pmol/L vs.（10.4 ± 2.1）pmol/L，t = 6.649，P < 0.001]、TSH[1.16（0.56，2.13）mIU/L vs. 0.48（0.15，1.12）mIU/L，Z = 3.532，P = 0.001]水平均显著降低，而两组患者间TT、FIB、PLT、MPV、PDW、LC的比较，差异均无统计学意义（P均> 0.05）。Spearman相关性分析显示，ESS患者血清TT3、FT3与PT（r = -0.337，P < 0.001；r = -0.321, P < 0.001）、APTT（r = -0.429，P < 0.001；r = -0.401，P < 0.001）、D-D（r = -0.405，P < 0.001；r = -0.338，P < 0.001）均呈负相关，TT3与PLT呈正相关（r = 0.184，P = 0.041）；TT4、FT4与PT（r = -0.369，P < 0.001；r = -0.223，P = 0.013）、APTT（r = -0.463，P < 0.001；r = -0.364，P < 0.001）、D-D（r = -0.310，P = 0.001；r = -0.273，P = 0.002）均呈负相关，与PLT均呈正相关（r = 0.227，P = 0.011；r = 0.273，P = 0.002）；TSH与APTT、D-D均呈负相关（r = -0.270，P = 0.002；r = -0.222，P = 0.012）。结论:ESS患者的血液处于低凝状态，甲状腺激素水平与凝血功能相关指标存在一定相关性。

目的 基于网络药理学预测三七治疗幽门螺杆菌(Hp)相关疾病机制,研究三七中有效活性成分人参皂苷Rb3对Hp造成的胃上皮细胞损伤的保护作用及机制.方法 使用Herb数据库收集"三七"的相关预测靶点,使用Gene Cards数据库收集Hp相关疾病的靶点;使用Draw Venn Diagram网站绘制Venn图,得到靶点交集;进行蛋白互作(PPI)网络分析、基因本体(GO)和京都基因与基因组百科全书(KEGG)富集分析.将GES-1细胞分为对照组、模型组及人参皂苷Rb3低、中和高浓度(1、5、10 μmol·L-1)组,人参皂苷Rb3组使用相应浓度的人参皂苷Rb3预处理,培养过夜12h至融合度为70％～80％.Hp悉尼株1(SS1)按感染复数(MOI)100加入细胞中制备损伤模型,人参皂苷Rb3继续给药,共培养48h.对照组不加SS1,对照组和模型组不加药.改良吉姆萨染色后通过光学显微镜观察细胞形态;结合Hoechst 33342荧光染色和Annexin V/PI双染流式细胞术检测细胞凋亡;试剂盒法检测活性氧(ROS)水平;采用实时荧光定量PCR(qRT-PCR)检测凋亡相关基因 TP53、Bax、Bcl-2 表达量;Western blotting法检测 P53、p-Akt、cleaved/pro-Caspase 9、Bcl-2、Bax、cleaved/pro-Caspase3的蛋白表达情况.结果 网络药理学结果表明三七治疗Hp相关疾病的靶点共16个,其PPI网络分析得到按度值大小排名前6位靶点为TP53、CASP3、PTGS2、IL6、TNF、IL1β.GO富集分析与KEGG富集分析结果均显示与凋亡相关.与模型组比较,经人参皂苷Rb3处理后,GES-1细胞的细胞核染色质致密深染,破裂的细胞逐渐减少;Hoechst 33342荧光染色细胞核强荧光数目明显减少;细胞凋亡率显著降低(P＜0.05);ROS水平显著降低(P＜0.05);TP53与Bax的mRNA水平显著降低,Bcl-2 mRNA水平显著升高(P＜0.05);p-Akt、Bcl-2蛋白表达显著升高(P＜0.05),P53、Bax、cleaved/pro-Caspase 9与cleaved/pro-Caspase 3蛋白表达显著降低(P＜0.05).结论 三七可能通过包括炎症及凋亡在内的多种途径治疗Hp相关疾病,人参皂苷Rb3对Hp诱导的胃上皮细胞凋亡发挥显著改善作用,其可能机制是降低氧化应激水平,并调节Akt的磷酸化和P53的表达.

目的 通过幽门螺杆菌(Hp)感染小鼠建立Hp相关胃炎模型,探讨猪苓多糖的保护作用及机制.方法 将C57BL/6小鼠随机分为4组:对照组、模型组、猪苓多糖(250mg,kg-1)组、核转录因子-κB(NF-κB)通路的抑制剂——吡咯烷二硫代甲酸铵(PDTC,阳性对照,100mg·kg-1)组.除对照组外,其余各组小鼠ig给予Hp悉尼株1(SS1)菌液(1×109CFU·mL-1),第1天每只0.4 mL,以后连续3 d每天igl次,每次0.2 mL.igHp完成4周后,猪苓多糖组和PDTC组给予相应剂量的药物,对照组和模型组小鼠给予无菌水,每只0.4 mL,每天1次持续14 d.将胃取出,沿胃大弯切开,肉眼观察胃黏膜变化;吉姆萨染色验证Hp在小鼠胃黏膜的定植;HE染色观察小鼠胃黏膜组织的炎症浸润状态;免疫组化检测核因子-κB(NF-κB)p65的表达;Western blotting法检测小鼠胃腺组织炎症因子白细胞介素-8(IL-8)蛋白表达;酶联免疫吸附法(ELISA)检测小鼠血清中IL-8的表达.结果 与模型组比较,猪苓多糖组小鼠胃黏膜褶皱整齐,出血点消失,黏膜光滑,胃黏膜颜色红润有光泽;炎症细胞浸润和其他组织损伤明显减少;细菌定植数量明显减少;胃上皮细胞中NF-κB p65的表达减弱;胃腺组织IL-8蛋白表达水平显著降低(P＜0.001);小鼠血清中IL-8表达水平显著降低(P＜0.001).结论 猪苓多糖可能通过抑制炎症信号通路NF-κB 相关分子的表达在 Hp 相关胃炎中发挥保护作用.

目的 目前有报导发现猪苓多糖可以降低炎性浸润的表达,但对Hp引起的胃黏膜上皮细胞炎症是否同样具有保护作用尚不得知.研究猪苓多糖(PPS)对幽门螺杆菌(Hp)诱导的人胃黏膜上皮细胞系(GES-1)的抗炎作用及相关机制.方法 细胞分组:①Hp与GES-1细胞共培养:分别设置对照组、M50组,M100组、M200组,对照组不做处理,其余各组分别按照MOI 50、100、200向人胃黏膜上皮细胞(GES-1)中加入Hp菌液,与之共培养;②加入猪苓多糖干预:分别设置空白组、模型组、Hp+猪苓多糖低、中、高浓度组,药物浓度分别为1.25、2.5、5 mg/mL,分别记作PPS-L组、PPS-M组、PPS-H组,以NF-κB通路抑制剂吡咯烷二硫代甲酸铵(Pyrrolidinedithiocarbamate ammonium,PDTC)作为阳性对照组,药物浓度为100μmol/L,记作PDTC组.运用RT-qPCR、Western blot检测白细胞介素8(IL-8)及核转录因子-κB(NF-κB)的基因及蛋白表达变化.结果 M50、M100、M200各组的炎症因子IL-6、IL-8在Hp感染的GES-1的表达明显高于对照组(P<0.05);与对照组相比,48 h后M50、M100、M200各组P65的表达升高(P<0.05).IκBα在48 h时表达量(1.246±0.279、1.118±0.123、1.102±0.076)较对照组(1.657±0.074)降低(P<0.05),各组的NF-κB及P65的mRNA表达量在共培养48 h时升高(P<0.05),且表达趋势呈浓度依赖性.加入猪苓多糖和PDTC干预后,与模型组对比,猪苓多糖各个浓度组及PDTC组的IL-6、IL-8及P65的表达明显降低(P<0.05),IκBα的表达量升高(P<0.05).细胞免疫荧光显示,与模型组相比,PPS-M和PDTC组P65入核的细胞个数明显减少(P<0.05).结论 PPS可能通过抑制NF-κB信号通路对Hp感染的GES-1细胞发挥炎症保护作用.

目的:观察柴朴汤联合化痰消瘀方治疗胃癌前病变伴焦虑抑郁(脾虚肝郁证)患者的临床疗效.方法:68例胃癌前病变伴焦虑抑郁状态(脾虚肝郁证)患者按随机数字表法分为对照组33例和治疗组35例.两组患者均给予抑制胃酸、保护胃黏膜、促胃肠动力、改善消化、补充叶酸和抗焦虑等西医常规疗法.治疗组在常规治疗的基础上给予柴朴汤联合化痰消瘀方,两组疗程均为6个月.治疗后,比较两组患者治疗前后中医证候积分、汉密尔顿焦虑量表(Hamilton anxiety scale,HAMA)和汉密尔顿抑郁量表(Hamilton depression scale,HAMD)评分、胃镜下黏膜病理积分,并比较两组患者HA-MA和HAMD疗效.结果:①胃镜下黏膜病理积分:治疗后,两组患者内镜下胃黏膜萎缩评分、肠化评分、异型增生评分均显著降低(P＜0.05),治疗组胃黏膜萎缩评分、肠化评分低于对照组(P＜0.05).②中医证候积分:治疗后,两组患者脘胀纳呆、胁下满痛、反酸欲呕、烦躁不安、咽中异物感、便溏不爽、舌质暗脉弦数等证候评分均显著下降(P＜0.05),治疗组胁下满痛、反酸欲呕、烦躁不安、咽中异物感评分低于对照组(P＜0.05).③HAMA和HAMD评分:治疗后,两组患者HAMA和HAMD积分显著降低(P＜0.05),治疗组HAMA和HAMD积分低于对照组(P＜0.05).④HAMA和HAMD疗效:治疗后,治疗组HAMA疗效的有效率为88.57％ (31/35),对照组为72.73％ (24/33),治疗组HAMD疗效的有效率为91.43％ (32/35),对照组为75.76％ (25/33),治疗组HAMA和HAMD疗效均优于对照组(P＜0.05).结论:柴朴汤联合化痰消瘀方治疗胃癌前病变伴焦虑抑郁(脾虚肝郁型)患者疗效显著,可有效降低胃黏膜内镜病理萎缩和肠化积分,改善患者焦虑抑郁状态.

目的:观察自拟方疏肝益胃汤治疗肝胃气滞型慢性萎缩性胃炎的临床疗效.方法:80例肝胃气滞型慢性萎缩性胃炎伴肠上皮化生及(或)异型增生的患者随机分为治疗组与对照组,每组40例.对照组予胃复春片及氟哌噻吨美利曲辛片口服,治疗组予中药汤剂疏肝益胃汤治疗,2组疗程均为6个月.观察并比较2组患者治疗前后症状(胃脘胀满或疼痛、胁肋胀痛、胸闷不舒、嗳气)积分、病理(萎缩、肠化生、异型增生)积分变化情况,疗程结束后比较证候疗效、病理疗效.结果:治疗后2组患者各项症状积分及病理积分均明显低于治疗前(P<0.05),治疗组上述积分均明显低于对照组(P<0.05).治疗组证候疗效总有效率为95.0％,明显高于对照组的60.0％(P<0.05).治疗组病理疗效总有效率为77.5％,明显高于对照组的57.5％(P<0.05).结论:常规药物治疗与中药汤剂疏肝益胃汤治疗均能明显改善肝胃气滞型慢性萎缩性胃炎伴肠上皮化生及(或)异型增生患者中医证候及胃黏膜病理状况,中药汤剂疗效更佳.

Ras-related Protein Rap1b, a GTP-binding protein belonging to the proximal RAS, which affects tumor progression through regulating tumor cell proliferation, invasion and participates in the functions of various immune cells. However, the potential roles and mechanisms of Rap1b in tumor progression and immunology remains unclear. In this study, we systematically analyzed the pan-cancer expression and prognostic correlation of Rap1b based on GTEX, CCLE, Oncomine, PrognoScan, Kaplan-Meier plotters and TCGA databases. The potential correlations of Rap1b with immune infiltration were revealed via TIMER and TCGA database. SangerBox database was used to analyzed the correlations between Rap1b expression and immune checkpoint (ICP), tumor mutational burden (TMB), microsatellite instability (MSI), mismatch repairs (MMRs) and DNA methylation. The results indicated that the expression level of Rap1b varies in different tumors. Meanwhile, the expression level of Rap1b strongly correlated with prognosis in patients with tumors, higher expression of Rap1b usually was linked to poor prognosis in different datasets. Rap1b was correlated closely with tumor immunity and interacted with various immune cells in different types of cancers. In addition, there were significant positive correlations between Rap1b expression and ICP, TMB, MSI, MMRs and DNA methylation. In conclusion, the results of pan-cancer analysis showed that the abnormal Rap1b expression was related to poor prognosis and tumor immune infiltration in different cancers. Furthermore, Rap1b gene may be used as a potential biomarker of clinical tumor prognosis.

取艾叶150克,鸡蛋3个,将艾叶洗净、切碎;鸡蛋打在碗里拌匀,加入艾叶搅匀,在铁锅里放油,待油烧热后将艾叶蛋液放入,炒至半熟时,加水200毫升,煮沸5分钟即成,待温度适宜时,渣水共服.一般30分钟后胃疼痛症状可明显减轻,隔4小时再按上方服1次可痊愈. 中医认为,艾叶具有散寒止痛、温经止血的功效,内服多用于治疗妇科病,外用常用于治疗皮肤瘙痒等症.现代药理研究表明,艾叶有抗菌、保护胃黏膜、利胆以及缓解平滑肌痉挛的作用.

目的:观察化痰消瘀方加味治疗胃食管反流病(GERD)伴慢性萎缩性胃炎(CAG)的疗效.方法:选取反流性食管炎(RE)或非糜烂性反流病(NERD)同时伴有CAG的70例患者为研究对象.按随机数字表法分为2组,每组各35例.对照组采用西医抑酸、促胃动力治疗,治疗组在对照组治疗基础上加用化痰消瘀方加味.治疗后观察比较2组患者的中医证候疗效、萎缩治疗总有效率、GERD治疗总有效率、汉密尔顿抑郁量表(HAMD)评分、汉密尔顿焦虑量表(HAMA)评分、匹兹堡睡眠质量指数(PSQI)评分.结果:疗程结束后,治疗组中医证候各项积分明显低于对照组(P＜0.05);2组胃黏膜萎缩治疗总有效率分别为88.57％、65.71％,治疗组明显高于对照组(P＜0.05);2组GERD治疗总有效率分别为82.86％、68.57％,治疗组明显高于对照组(P＜0.05);2组HAMD、HAMA、PSQI评分较治疗前均降低(P＜0.05),且治疗组积分明显低于对照组(P＜0.05).结论:化痰消瘀方加味治疗GERD伴CAG的疗效优于单纯使用常规西医治疗,值得临床推广.

目的:采用血清代谢组学探讨香砂六君合半夏泻心汤治疗糖尿病胃轻瘫大鼠的作用机制.方法:除正常组外,其余大鼠给予腹腔注射链脲佐菌素及高脂饲料喂养建立糖尿病胃轻瘫大鼠模型.大鼠模型成功建立后随机分为模型组、莫沙比利组(1.56 mg·kg-1)及香砂六君合半夏泻心汤组(9.3 g· kg-1).给予药物干预8周后,测定各组大鼠胃残留率;收集大鼠血清样本,采用GC-MS技术对血清样本进行高分辨质谱检测,应用PLS-DA多元模式进行血清代谢轮廓的比较以及生物标志物的鉴定,运用MetPa数据库分析相关代谢通路.结果:与正常组相比,模型组的胃残留率显著升高(P＜0.01);香砂六君合半夏泻心汤组和莫沙必利组的胃残留率较模型组明显降低(P＜0.05).血清代谢组学结果显示:正常组和模型组的代谢轮廓具有明显的差异,香砂六君合半夏泻心汤组的代谢轮廓趋近正常组,并对血清中N-乙酰天门冬氨酸、葡萄糖-1-磷酸、塔格糖、3-6脱水-D-半乳糖、木糖醇和脯氨酸等13个生物标志物具有明显的回调作用,并筛选出2条相关的代谢通路.结论:香砂六君合半夏泻心汤对糖尿病胃轻瘫大鼠有一定改善胃动力作用,其作用机制可能与通过回调多种血清代谢产物的含量及调控多条代谢通路等相关.

目的:基于网络药理学预测和胃癌前病变(PLGC)大鼠模型验证的方法,探讨化痰消瘀方治疗胃癌前病变的分子机制.方法:利用网络药理学技术筛选化痰消瘀方治疗胃癌前病变的关键活性成分及其作用靶点,并进行蛋白质间相互作用分析,GO功能富集和KEGG通路富集.建立PLGC大鼠模型,给予化痰消瘀方干预治疗12 w,苏木精-伊红染色法观察大鼠胃黏膜组织的病理学改变,AB-PAS染色法观察大鼠胃黏膜组织的肠上皮化生病理改变,免疫组化法对预测结果中PI3K/Akt信号通路的相关蛋白表达进行分析.结果:网络药理学结果显示:化痰消瘀方含有98个活性成分,作用于129个靶点,主要涉及酶结合、药物反应、细胞凋亡调控等生物学途径以及PI3K/Akt、TNF等信号通路.动物实验验证结果显示:与模型对照组比较,化痰消瘀方干预治疗后可改善PLGC大鼠胃黏膜组织病理学改变,并减轻肠上皮化生等病理改变,PI3K/Akt信号通路中相关蛋白p-Akt、p-PI3K、mTOR表达下调,PTEN表达上调.结论:化痰消瘀方通过多成分、多靶点、多通路共同作用治疗PLGC,其中PI3K/Akt信号通路是其作用的主要通路之一.

目的 探究化痰消瘀方与常规西药治疗胃癌癌前病变的疗效.方法 随机选取200例入院接受治疗的胃癌癌前病变患者,按照随机数字表法分为对照组和观察组,每组100例,分别给予常规西药、化痰消瘀方治疗,对比两组患者治疗前后症状评分、肿瘤标志物及病理肠化逆转率变化.结果 治疗后观察组口渴的症状评分(0.44±0.12)分、胃脘疼痛(0.37±0.09)分、大便溏(0.39±0.08)分、胃脘胀满(0.29±0.08)分明显低于对照组(0.95±0.32)分、(0.89±0.55)分、(0.88±0.38)分、(0.84±0.31)分(P＜0.05);治疗后观察组患者的CA125(15.77±1.53) U/mL、CA19-9(31.11±3.07)U/mL、CA72-4(4.90±0.33) U/mL及CEA含量(1.34±0.35) ng/mL明显低于对照组(28.64±2.20) U/mL、(42.44±4.85) U/mL、(10.49±1.88) U/mL、(2.91±0.45) ng/mL(P ＜0.05);观察组患者的治疗后3个月、6个月、1年的病理肠化逆转率(52.00％)、(63.00％)、(78.00％)明显高于对照组3个月(34.00％)、6个月(49.00％)、1年(58.00％)的(P＜0.05).结论 化痰消瘀方治疗胃癌癌前病变效果显著,症状缓解,降低肿瘤标志物水平,增加病理肠化逆转率.

[目的]观察蒲地蓝消炎口服液联合四联疗法(PPI+胶体果胶铋+阿莫西林+呋喃唑酮)治疗常规四联疗法(PPI+胶体果胶铋+阿莫西林+克拉霉素)杀菌失败的慢性萎缩性胃炎伴幽门螺杆菌(Hp)感染的临床疗效.[方法]将155例慢性萎缩性胃炎伴Hp感染且曾使用常规四联疗法治疗但杀菌失败的患者随机分为观察组(78例)和对照组(77例),并将观察组依据患者自身中医症候分为湿热证型和肝胃不和证型.对照组予以雷贝拉唑、阿莫西林胶囊、呋喃唑酮片、胶体果胶铋胶囊四联疗法根除Hp,观察组在对照组基础上加用蒲地蓝消炎口服液,每组疗程均为2周.疗程结束4周后复查Hp,评估每组患者Hp根除疗效.[结果]观察组总有效率为88.46％,对照组为72.73％,观察组较对照组效果更佳,差异有统计学意义(P＜0.05).观察组中湿热证型有效率为97.5％,而肝胃不和证型有效率为78.95％,二者之间疗效比较差异有统计学意义(P＜0.05).[结论]蒲地蓝消炎口服液联合四联疗法根除Hp的疗效优于单纯四联疗法,且对湿热型患者根除Hp的效果更佳,症状改善显著,值得临床应用推广.

目的 比较化痰消瘀加减方和西药常规方案治疗胃癌前期病变(PLGC)的临床疗效.方法 将82例慢性萎缩性胃炎(CAG)伴异型增生(Dys)和肠上皮化生(IM)的患者随机分为2组,每组41例.治疗组给予化痰消瘀加减方治疗,对照组采用常规西药口服治疗,疗程为6个月.观察2组临床疗效、中医证候积分以及胃镜病理积分情况.结果 治疗组临床总有效率为92.68％,高于对照组的73.17％,差异有统计学意义(P＜0.05);治疗后,2组中医证候(胃痛、纳差、暖气、反酸、痞满、嘈杂)评分均较治疗前降低,且治疗组各证候积分低于对照组,差异有统计学意义(P＜0.05);治疗后,2组病理积分(萎缩、IM、Dys)均较治疗前降低,且治疗组以上积分均低于对照组,差异有统计学意义(P＜0.05).结论 化痰消瘀加减方治疗PLGC疗效显著,可有效改善患者临床症状,降低萎缩、IM及Dys病理评分,甚至逆转PLGC病情.与常规口服西药治疗方案比较,化痰消瘀加减方具有明显治疗优势,且临床疗效安全可靠.