Mechanism underlying the protective effect of Kaixin Jieyu Fang on vascular depression following cerebral white matter damage

The Chinese compound Kaixin fieyu Fang can be used to treat vascular depression; however, the underlying mechanism remains unclear. This study established a rat model of chronic cerebral ischemia-caused white matter damage by ligation of the bilateral common carotid arteries. Rats received daily intragastric administration of a suspension of Kaixin ]ieyu Fang powder. After 3, 7 and 21 days of treatment, the degree of white matter damage in the cerebral ischemia rat model was alleviated, Bcl-2 protein and mRNA expression in brain tissue increased, and Bax protein and mRNA expression decreased. These results indicate that Kaixin Jieyu Fang can alleviate cere- bral white matter damage, and the underlying mechanism is associated with regulation of Bcl-2/ Bax protein and mRNA expression, which is one of possible mechanism behind the protective effect of Kaixin Jieyu Fang against vascular depression.

Kaixin001 Network with Random Hierarchical Model

A new random hierarchical model to describe the neighborhood properties of Kaixin001 network is developed in this paper. The degree distribution of this network model follows P（k） k-γ with y = 1. It means the network model has a power-law distribution. Through calculating the clustering coefficients and average path length （APL）, the result reflects that the model has the properties of high clustering coefficients and low APL.

The treatment effects of Kaixin Powder on depression through heart-spleen axis

Depression is a kind of mental disorder characterized by conspicuous and persistent low mood, sustained sadness, loss of interest and forgetfulness. In traditional Chinese medicine, heart (different from the concept in Western medicine) control the emotions. Overthinking hinders the function of the spleen. Deficiency of spleen leads to lack of heart-Qi. Deficiency of the spleen also leads to dysfunction of heart. Once the heart is dysfunction, Qi will be stagnated in Danzhong(thoracic center), eventually leads to depression. In Traditional Chinese medicine, the development of depression is a heart-spleen-heart process, which can be called the "heart-spleen axis". Biomedicine studies have found that the progress of depression is mainly caused by long-term adverse stimulation of the central nervous system, which affects the Hypothalamic-pituitary-adrenal axis (HPA) to convey monoamine neurotransmitters, such as 5- hydroxytryptamine (5-HT), and further damaged the intestinal mucosal barrier, increased its permeability, and produced a large number of lipopolysaccharides (LPS) and inflammatory factors. The production of LPS and inflammatory cytokines reduces the synthesis of 5-HT by consuming tryptophan, and the decrease of 5-HT in serum results in the decrease of 5-HT levels in the brain. At the same time, changes in the intestinal microbiota alter the concentration of brain-derived neurotrophic factor (BDNF) via the vagal pathway, ultimately creating a vicious brain-gut- brain cycle. Kaixin Powder has the effect of invigorating spleen and eliminating dampness, awaking consciousness and inducing resuscitation, and can adjust the imbalance of gut microbiota and neurotransmitters to achieve the purpose of treating depression.

Effects of Kaixin Jieyu Decoction(开心解郁汤)on Behavior, Monoamine Neurotransmitter Levels, and Serotonin Receptor Subtype Expression in the Brain of A Rat Depression Model

Objective： To determine the mechanisms underlying the anti-depressant effects of Kaixin JieyuDecoction （开心解郁汤, KJD） by investigating the effects of KJD on behavior, monoamine neurotransmitterlevels, and serotonin （5-HT） receptor subtype expression in the brain in a rat model of depression. Methods：The rat depression model was established using chronic unpredictable mild stress （CUMS）. Forty-eight SpragueDawley rats were randomly divided into control, depression model （CUMS）, CUMS＋KJD （7.7 g/kgl-d1 ofcrude drug）, and CUMS＋fluoxetine （2.4 mg/kgl.d1） groups （n=12 in each group）, and the treatments lastedfor 21 days. We regularly evaluated body weight, sucrose consumption, and horizontal and vertical activityscores in open-field tests. The content of the monoamine neurotransmitters 5-HT, norepinephrine （NE）, anddopamine （DA） and the DA metabolite homovanillic acid in the cerebral cortex, and 5-HT1A and 5-HT2A receptormRNA in the cerebral cortex and the hippocampus, were determined respectively by high-performance liquidchromatography-coularray electrochemical detector and real-time polymerase chain reaction. Results： Comparedwith the control group, CUMS rats showed a variety of depression-like behavioral changes, including a significantreduction in body weight, sucrose consumption, and horizontal and vertical activity scores in open-field tests（P〈0.05 or ,P〈0.01）, and a significant decrease in 5-HT and NE levels and 5-HT2A receptor mRNA expression.In contrast, they showed a significant increase in 5-HT1A receptor mRNA expression in the cerebral cortex. Inthe hippocampus, 5-HT1A receptor mRNA expression was lower whereas 5-HT2A receptor mRNA expressionwas higher than in the control group （P〈0.05 or P〈0.01）. Treatment with KJD or fluoxetine partially attenuatedthese changes （,P〈0.05 or ,P〈0.01）. Conclusion： KJD could normalize the levels of 5-HT and NE and adjust thebalance of 5-HT2A and 5-HT2A receptor expression in rat cerebrum, and this may be one of mechanisms ofantidepressant effects of KJD.

Effects of Kaixin Powder(开心散)on Melatonin Receptor Expression and ^(125)I-Mel Binding Affinity in A Rat Model of Depression

Objective： To explore the effects of Kaixin Powder （开心散, KXP） on melatonin receptor （MR） expression and 1261-Mel binding affinity in a depression rat model. Methods： Seventy-two male Wistar rats were divided into six groups： a blank control group, model group, ramelteon group, KXP high-dosage group （HKXP）, medium-dosage group （MKXP） and low-dosage group （LKXP）. To establish the depression model, all groups except the blank control group were singly housed and exposed to chronic unpredictable mild stress. Weight gain, sucrose consumption and the open-field test were used to evaluate induction of depression. KXP at 260, 130 and 65 mg/（kg·d） was also respectively administered to the rats in the HKXP, MKXP and LKXP groups for 21 days. Ramelteon [0.83 mg/（kg·d）] was given to the positive drug control group. An equivalent volume of physiological saline was given to the blank and model groups. The liquid chip method was used to measure the concentration of plasma melatonin （MT）. Mell a （MT1） and Mellb （MT2） expression levels were determined by Western blotting. In addition, a radioactive ligand-binding assay was used to analyze the specific binding properties and dynamic characteristics between MR and 125I-Mel. Results： The results of weight gain, sucrose consumption and the open-field test showed that our model successfully produced depressive symptoms and depressive-like behavior. The concentration of plasma MT in the model group decreased significantly at night but increased in the MKXP group （P〈0.05）. The HKXP group showed significantly increased expression of MT1 （P〈0.05）; however, the expression of MT2 in all groups exhibited no significant differences （P〉0.05）. The maximum binding capacity （Bmax） for specific binding between MR and 125I-Mel in the MKXP group was significantly higher than that in the model group （P〈0.05）, but no significant differences were found in the equilibrium dissociation constant （Kd） of each group （P〉0.05）. Conclusions： KXP may have a similar effect as ramelteon. KXP improved depressive-like behavior by increasing the concentration of plasma MT and MT1 expression, thereby increasing three Bmax of MR tO achieve the desired antidepressant effect.

Effects of Kaixin Jieyu Decoction (开心解郁汤) on Behavior and Glial Fibrillary Acidic Protein Expression in Cerebral Hippocampus of A Rat Vascular Depression Model

Objective：To explore the effects and anti-depression mechanisms of Kaixin Jieyu Decoction（开心解郁汤,KJD）.Methods：The rat vascular depression（VD） model was established by ligation of bilateral common carotid arteries（LBCCA） combined with chronic unpredictable mild stress（CUMS）.Forty Wistar rats were randomly divided into sham,VD model,VD ＋ high-dose KJD[15.4 g/（kg·d） of crude drug],VD ＋ medium-dose KJD[7.7 g/（kg·d） of crude drug],and VD ＋ fluoxetine[2.4 mg/（kg·d）]groups（r〉=8 in each group）,and the treatments lasted for 21 days.Changes of behavior and hippocampus pathology were observed.The level of glial fibrillary acidic protein（GFAP）protein and mRNA in hippocampus was detected respectively by immunohistochemistry and real-time polymerase chain reaction.Results：Compared with the sham group,rats in model group showed a variety of behavioral obstacles,including a significant reduction in sucrose consumption percentage,horizontal and vertical activity scores in open-field tests（P〈0.05 or P〈0.01）,pathological damage like neuronal degeneration,necrosis,and a significant decrease of GFAP protein and mRNA in hippocampus（P〈0.01）;compared with the model group,rats in the high-dose KJD group,medium-dose KJD group and fluoxetine group obtained notable higher behavioral scores,and pathological injury lessened in hippocampus with a increased expression of GFAP protein and mRNA（P〈0.05 or P〈0.01）;compared with the medium-dose KJD group and fluoxetine group,GFAP mRNA in highdose KJD group expressed higer（P〈0.05）.Conclusion：LBCCA combined with CUMS may cause depression-like behavioral changes resulting in the VD model of rats whose depression state can be ameliorated by KJD,and the mechanism of cerebral protection is related possibly with promoting expression of GFAP in hippocampus.

New insights into effects of Kaixin Powder on depression via lipid metabolism related adiponectin signaling pathway

Objective:To clarify the anti-depressive potential mechanisms of Kaixin Powder(KP),a drug that helps to prevent and treat depression and other mentaldiseases,from genome-wide transcriptome profiling.Methods:Transcriptome and KEGG pathway analysis were conducted on the hippocampus of depressed rats,then the differentially expressed genes were validated and serum concentration of lipid parameters were identified by enzymatic assays.Furthermore,high-fat diets induced depression-like behaviors in Syrian golden hamsters were conducted to verify the predicted molecular mechanisms acquired from the transcriptome analysis.Results:Transcriptome results revealed that the 24 differentially expressed genes(DEGs)in chronic mild stress(CMS)rats could be reversed after two weeks of KP treatment.The mechanisms of KP in treating depression firstly involved the regulation of several pathology modules,including lipid metabolism,synapse function and inflammation.KP could regulate imbalances of lipid homeostasis in high-fat diet induced depressive symptoms.Furthermore,it was validated that cholesterol metabolism dysfunction can be ameliorated by KP,which was correlated with upregulation of the AdipoR1-BDNF(brainderived neurotrophic factor)co-regulatory pathway.Conclusion:Taken together,our results demonstrated that KP not only alleviates depression via traditional mental illness targets,but it may also simulates the cholesterol metabolism and adiponectin signaling with multi-target characteristics.

Clinical Observation on Effect of Kaixin Capsule (开心胶囊) in Treating 40 Patients with Diabetic Myocardial Ischemia

Objective： To observe the effect of Kaixin Capsule （开心胶囊, KXC） on myocardial ischemia and plasma endothelin （ET） level in patients with diabetic heart disease （DHD）. Methods： The 72 subjects for observation were randomly selected from inpatients whose diagnosis fit to the standard of DHD. The 32 patients allocated in the control group were treated with conventional Western medicine, and the 40 patients in the treated group were treated with conventional Western medicine in combination with KXC, with the therapeutic course for both groups as 60 days. Results： On ECG, the total effective rate and markedly ef- fective rate in the treated group was 85. 0% and 37. 5% respectively, higher than those in the control group＇s 68.7% and 28. 1% respectively, and showing significant difference between the two groups （P〈 0.05）. The level of ET in patients in both groups was significantly higher than normal range, after treatment, but reduced to different extent, and the comparison between them also showed that the difference was significant （P〈0.05）. Conclusion： KXC might, by way of inhibiting and blocking the release of ET, lower its level in plasma so as to improve the myocardial ischemic condition of patients with DHD.

Effects of Kaixin Powder on Expression of 5-HT Receptor in Hippocampus of Depressed Rats Induced by CUMS

Objective To observe the influence of Kaixin Powder on ethology,content of 5-HT in the hippocampus, expression of m RNA, and protein in 5-HT1 A and 5-HT2 A receptors in the hippocampus of depressed rats induced by chronic unpredictable mild stress（CUMS）. Methods Twenty-four male Wistar rats were randomly divided into blank,model, Trazodone, and Kaixin Powder groups, six rats in each group. In addition to the blank control group, other groups were established the depression model induced by CUMS combined with isolated feeding. At the same time, Trazodone group and Kaixin Powder group were treated with corresponding drugs for 3 weeks. After 3 weeks of administration, the rats were sacrificed, and a series of indexes were measured such as the contents of 5-HT, m RNA expression levels of 5-HT1 A and 5-HT2 A receptors, protein expression levels of 5-HT1 A and 5-HT2 A receptors, and so on. Results A series of indexes in the model group were decreased significantly such as the body weight growth, the sugar water intake, the score of Open Field Test, the content of5-HT in the hippocampus, expression of m RNA, and protein in 5-HT1 A receptor, while the expression of m RNA and protein in 5-HT2 A receptor were increased significantly.Compared with the model group, the indexes were ameliorated in Trazodone and Kaixin Powder groups. Kaixin Powder is better than Trazodone in decreasing the level of protein in 5-HT2 A receptor. Conclusion The result indicated that the depression performance of depressed rats induced by CUMS can be ameliorated by Kaixin Powder,and the mechanism maybe concerned with increasing the contents of 5-HT, exciting 5-HT1 A receptor, and antagonising 5- HT2 A receptor.

Clinical Observation of Kaixin Capsule (开心胶囊) in Treating Type 2 Diabetes Mellitus Complicated with Abnormal Lipidemia

Objective: To observe the clinical efficacy of Kaixin Capsule (KXC, 开心胶囊), a Chinese compound preparation, in treating type 2 diabetes mellitus (DM) complicated with abnormal lipidemia. Methods: Seventy-two DM inpatients were medicated on the basis of administering conventional hypoglycemics, and KXC was orally taken. They were compared with those patients only taking hypoglycemics to observe the change of blood lipid before and after treatment. Results: The total cholesterol of KXC combined with hypoglycemics group had their blood lipid lowered by 14% after treatment and triglyceride lowered by 36%, HDL-C raised by 11%, and LDL-C lowered by 24%. Compared with only hypoglycemics treatment, there was significant difference (P<0.01). Conclusion: KXC has good blood lipid regulating effect on DM complicated with abnormal lipidemia.

开心散治疗乳腺癌失眠症患者的临床疗效及对血清5-羟色胺水平的影响

目的观察开心散治疗乳腺癌失眠症患者的临床疗效及对血清5-羟色胺(5-hydroxytryptamine,5-HT)水平的影响。方法将63例乳腺癌失眠症患者随机分为对照组33例和治疗组30例。对照组患者采用艾司唑仑治疗,治疗组患者采用开心散联合艾司唑仑治疗。比较两组治疗前后匹兹堡睡眠质量指数量表(Pittsburgh sleep quality index,PSQI)、抑郁自评量表(self-rating depression scale,SDS)、焦虑自评量表(self-rating anxiety scale,SAS)、欧洲癌症研究和治疗协作组编制的癌症患者生活质量评分(European organization for research and treatment of cancer quality of life questionnaire-core 30,EORTC QLQ-C30)以及血清5-HT水平;在连续治疗4周后,比较两组临床疗效及不良反应发生率。结果治疗4周后,两组PSQI、SDS、SAS评分均较治疗前显著降低(P<0.05),且治疗组PSQI评分显著低于对照组(P<0.05);治疗组EORTC QLQ-C30躯体功能、情绪功能、认知功能以及社会功能评分均显著高于对照组(P<0.05);两组患者治疗后血清5-HT水平较治疗前显著升高(P<0.05),且治疗组血清5-HT水平高于对照组(P<0.05);治疗组疗效优于对照组(P<0.05);治疗组总不良反应发生率低于对照组,差异有统计学意义(P<0.05)。结论相较于单纯艾司唑仑治疗,开心散联合艾司唑仑能更好地改善乳腺癌患者睡眠,升高血清5-HT水平,提高乳腺癌患者生活质量,降低不良反应发生率。

开心散改善小鼠肥胖相关认知障碍的机制研究

目的 观察开心散对肥胖相关认知障碍模型小鼠认知下降的改善作用,并探究其作用机制。方法 6周龄C57BL/6J雄性小鼠随机分为普通饮食、高脂饮食、开心散低剂量和开心散高剂量组各10只。通过长期(16周)高脂饮食方法复制肥胖相关认知障碍动物模型,造模13~16周期间,各组小鼠灌胃相应药物。16周后,应用Morris水迷宫评价各组小鼠的认知功能;ELISA法测定海马区白细胞介素(interleukin,IL)-6、肿瘤坏死因子(tumor necrosis factor,TNF)-α、IL-10及转化生长因子(transforming growth factor,TGF)β1浓度;免疫荧光法标记海马区M1型、M2型小胶质细胞;Western blot法测定海马区精氨酸酶(arginase,Arg)-1蛋白表达。结果 与普通饮食组小鼠比较,高脂饮食组小鼠体质量明显增加,逃避潜伏期明显延长,穿越平台区次数及平台区象限探索时间明显减少,海马区IL-6、TNF-α含量及M1型小胶质细胞明显增多(P<0.01),IL-10、TGF-β1、Arg-1含量及M2型小胶质细胞显著减少(P<0.01)。与高脂饮食组比较,开心散干预组小鼠体质量下降、认知功能明显改善,海马区IL-6、TNF-α含量及M1型小胶质细胞明显减少(P<0.05),IL-10、TGF-β1、Arg-1含量及M2型小胶质细胞显著增加(P<0.05),且开心散的干预作用呈现剂量依赖性。结论 开心散可通过减轻体质量及调控海马区小胶质细胞转化向M2型倾斜降低海马区炎症因子水平,进而改善高脂饮食诱导的肥胖相关认知障碍。

开心散调控自噬防治阿尔茨海默症研究进展

阿尔茨海默症(alzheimer disease,AD)是目前常见的一种神经退行性疾病,该病的发病率正处在一个持续上升的阶段,由于其发病机制复杂,因此对该病的治疗方案也有很多。随着对自噬研究的深入,发现在一定程度上调节自噬可以对AD产生影响并且一定程度上可以改善AD症状。开心散由唐代孙思邈创立,由人参、远志、茯苓、石菖蒲4味药组成,该方补泻兼施,以补为主,主要治疗心悸怔忡、失眠健忘等疾病。随着现代医学的发展,以及对其药物成分的深入研究,发现其在改善学习记忆方面具有显著效果,同时发现了开心散的药物成分可以通过影响自噬相关蛋白对AD进行调节。其中腺苷酸活化蛋白激酶(AMPK)自噬通路是这4味药发挥作用的主要通路。因此,该文通过查阅中外文献并进行整理分析,对开心散调控自噬防治AD做出综述,为阿尔茨海默症的临床治疗提供新思路。

开心散治疗抑郁症与抑郁合并心肌梗死差异机制网络药理学研究及关键靶点验证

目的:采用网络药理学方法探讨开心散治疗抑郁症和抑郁症合并心肌梗死(myocardial infarction,MI)的主要成分、作用靶点、传导通路和作用机制的异同并对关键靶点进行实验验证。方法:基于公共数据库结合ADME算法筛选开心散有效成分和作用靶点;通过DisGeNET数据库筛选抑郁症和MI及其共病靶点;利用STRING 11.0数据库构建蛋白-蛋白互作(protein-protein interactions,PPI)网络;通过核心靶基因导入基因功能注释数据库(the database for annotation,visualization and integrated discovery,DAVID)进行京都基因与基因组百科全书(kyoto encyclopedia of genes and genomes,KEGG)靶点相关通路分析;通过Cytoscape构建“药物成分-靶点-通路”网络;分析药物成分血脑屏障通过性,并采用Autodock Vina软件进行分子对接验证;建立抑郁症体外模型,采用蛋白质免疫印迹法(western blot,WB)对关键蛋白表达进行验证。结果:筛选出抑郁症与MI共同靶点28个;开心散主要成分30种,治疗抑郁症潜在靶点36个,其中关键靶点为Akt1、TNF、MAPK8、JUN、PTGS2、IL1B、IFNG、GSK3B、NOS2、DRD1等;开心散治疗抑郁症合并MI的主要成分14种,共同作用关键靶点为Akt1、TNF、IL1B、GSK3B、NOS2、BAX、NR3C2、NOS3、ESR1、ADRB1;开心散治疗抑郁症的成分较治疗抑郁症合并MI共同成分具有更强的血脑屏障通过性;分子对接结果显示山柰酚作用于Akt1靶点,参与调控PI3K/Akt通路;体外实验证实山柰酚可上调抑郁模型细胞Akt1蛋白表达。结论:开心散治疗抑郁症和抑郁症合并MI成分和靶点既有相同之处也有不同之处,体现“异病同治”的特点,且其治疗抑郁症主要侧重于对中枢神经系统和内分泌系统的调节,验证实验证实开心散对于治疗抑郁症和抑郁症合并MI具有有效性。

益气活血开心汤改善冠心病合并抑郁大鼠抑郁样行为作用机制研究

目的探讨益气活血开心汤是否通过p-CREB/BDNF途径改善大鼠冠心病(CHD)后抑郁症状以及是否能够抑制海马神经元的凋亡。方法将SD大鼠随机分为4组:空白组、模型组、中药组、西药组。采用结扎冠状动脉左前降支构建急性心肌梗死(AMI)模型,联合慢性不可预知刺激(CUMS)21 d构建CHD合并抑郁模型;同时,中药组、西药组分别给予益气活血开心汤、氟西汀灌胃21 d。通过大鼠整体状态、体质量、旷场实验、强迫游泳和蔗糖偏好实验评估抑郁样行为;尼氏染色观察海马神经元的形态结构和凋亡情况;Western blot和免疫荧光评估海马复合体CA1区磷酸化的环磷酸腺苷反应元件结合蛋白(p-CREB)和脑源性神经营养因子(BDNF)的表达。结果大鼠的抑郁样行为经过益气活血开心汤和氟西汀治疗后得到明显改善(P<0.05,P<0.01);海马CA1区的p-CREB和BDNF的表达明显增多(P<0.05)。结论结果表明,益气活血开心汤可以明显改善CHD后抑郁大鼠的抑郁症状和神经功能,并能够抑制海马神经元的凋亡情况,且与氟西汀的改善作用无显著差异。

经典名方开心散制剂工艺研究

目的:研究经典名方开心散提取制剂工艺,提高活性成分转移率,保证药品质量。方法:采用水蒸气蒸馏法提取石菖蒲挥发油,Box-Behnken实验设计方法优化所得挥发油包合工艺;以总多糖量、总皂苷量和出膏率为指标,通过均匀设计法确定后续水煎煮提取的料液比、时间和次数等条件。结果:确定β-环糊精与挥发油比例为6∶1,包合温度40℃,包合时间为80 min的包合工艺;水煎煮提取条件为料液比1∶12,提取时间3 h,提取次数3次。结论:该实验确定了开心散提取制剂工艺条件,挥发油成分转移率增加近94.94%。

高温瞬时灭菌对开心散有效成分含量及微生物学指标的影响

目的:比较不同高温瞬时灭菌条件下开心散的灭菌效果,结合灭菌后样品中有效成分含量的变化,确定最佳灭菌条件。方法:采用高温瞬时灭菌法对2~8目的远志、人参、茯苓和石菖蒲4味中药的粗颗粒进行灭菌,分别考察160、165、170℃3个温度水平,灭菌时间分别为5、7、9 s。在洁净区对灭菌粗颗粒分别进行粉碎,过六号筛后均匀混合,制得开心散。参照《中华人民共和国药典》2020年版进行微生物限度检测,并采用高效液相色谱法对开心散灭菌前后的样品进行含量检测。结果:9个灭菌条件下开心散样品的需氧菌总数均小于1×104CFU·g^(–1)、霉菌和酵母菌总数均小于1×102CFU·g^(–1)。同时,控制菌项下的大肠埃希菌、沙门菌、耐胆盐革兰阴性菌均未检出,所有开心散灭菌样品均符合口服散剂的微生物限度要求。开心散中8个有效成分(远志[口山]酮Ⅲ、3,6′-二芥子酰基蔗糖、细叶远志皂苷、人参皂苷Rg1、人参皂苷Rb1、茯苓酸、β-细辛醚和α-细辛醚)的含量受不同灭菌温度和时间影响。结论:结合需氧菌、霉菌和酵母菌、控制菌结果和有效成分含量变化情况,最终确定灭菌温度160℃、灭菌时间5 s为开心散最佳高温瞬时灭菌条件。

开心逍遥汤联合沙库巴曲缬沙坦治疗慢性心力衰竭合并高血压的临床效果

目的探讨开心逍遥汤联合沙库巴曲缬沙坦治疗慢性心力衰竭(CHF)合并高血压患者的临床效果。方法选取2022年2月至2023年12月驻马店市中医院收治的CHF合并高血压患者共计75例,以随机数字表法分成研究组(37例)与对照组(38例),对照组接受沙库巴曲缬沙坦治疗,研究组接受开心逍遥汤联合沙库巴曲缬沙坦治疗,比较两组临床疗效、血压水平、心功能、心肌损伤指标。结果研究组治疗总有效率(86.49%)较对照组(65.79%)更高(P<0.05);两组治疗后收缩压(SBP)、舒张压(DBP)水平下降(P<0.05),研究组较对照组更低(P<0.05);两组治疗后左室射血分数(LVEF)、心排血量(SV)升高(P<0.05),左心室质量指数(LVMI)下降(P<0.05),研究组LVEF、SV较对照组更高(P<0.05),LVMI更低(P<0.05);两组治疗后N末端B型脑钠肽前体(NT-proBNP)、肌钙蛋白(cTn)I、基质金属蛋白酶9(MMP-9)水平下降(P<0.05),研究组较对照组更低(P<0.05)。结论给予CHF合并高血压患者开心逍遥汤联合沙库巴曲缬沙坦治疗,能够提高临床效果,稳定血压水平,改善患者心功能及心肌损伤指标。

“开心”是非题

早在半年多前千橡推出kaixin.com时,就已埋下了关于两个开心网之争的种子。这场迟来的官司,会不会又是SNS的一次炒作?

开心散治疗轻、中度抑郁症临床观察

目的:观察开心散治疗抑郁症的临床疗效。方法:运用随机数字表法将80例轻、中度抑郁症患者分为治疗组和对照组,其中治疗组40例,用开心散治疗,对照组40例,用氟西汀治疗,疗程均为8周,运用HAMD量表总分减分率、HAMD量表七项因子减分值进行疗效评定。结果:在治疗2周、4周时,治疗组的HAMD减分疗效优于对照组(P<0.05),而两组在治疗6周、8周时HAMD减分疗效相当;在治疗8周时治疗组的临床控制率优于对照组(P<0.05)。治疗组对焦虑躯体化因子、睡眠障碍因子的减分值优于对照组,差异有统计学意义(P<0.05)。结论:开心散是治疗轻、中度抑郁症的安全、有效方剂,值得进一步深入研究。