QingReDu Capsule is commonly used clinically to treat psoriasis vulgaris, the mechanism of treating psoriasis vulgaris is still unclear. Using the ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS/MS), we analyzed the components in rat plasma after QingReDu Capsule administration. We then predicted the mechanistic pathways of QingReDu Capsule in ameliorating psoriasis vulgaris by screening the intersecting targets of the QingReDu Capsule plasma entry components and psoriasis vulgaris using network pharmacology and molecular docking. Combined with pharmacodynamic evaluation and HE staining, we investigated the efficacy and mechanism of QingReDu Capsule in treating psoriasis vulgaris. Forty-one compounds were identified in the rat plasma after QingReDu Capsule administration, thirty-seven QingReDu Capsule components with the InChI SMILES structure were screened, and two hundred and thirty-five targets intersected with psoriasis vulgaris. network pharmacology revealed that QingReDu Capsule is not only involved in the regulation of the inflammatory response, reactive oxygen species metabolism, and intracellular oxidative stress, but also related to the nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. The molecular docking results showed that 10 components, including Myristicin, had good affinity with the screened core targets. The pharmacodynamic results showed that QingReDu Capsule reduced the serum levels of tumor necrosis factor α (TNF-α), interleukin 17 (IL-17), and interleukin 23 (IL-23) by down-regulating the protein levels of enhancer of Zeste Homolog 2 (EZH2) and NF-κB, reduced erythema and the scaling of skin lesions, and treated histopathological damage to the skin, such as hyperkeratosis with keratosis imperfecta and the thickening of the sphenoid layer. These findings illustrated that QingReDu Capsule treat psoriasis vulgaris by affecting the EZH2/NF-κB signaling pathway and influencing the level of inflammatory factors.

Persicae Semen is an edible Chinese herbal medicine that ameliorates myocardial ischemia. However, its pharmacodynamic properties and mechanisms of action remain unclear. This study aimed to investigate the ameliorative effect of Persicae Semen extract (PS) on acute myocardial ischemia (AMI) in rats and explore its mechanism of action. After the PS administration to rats, 12 compounds were identified in the plasma. PS can significantly improve cardiac function, regulate creatine kinase (CK), creatine kinase MB (CK-MB), cardiac troponin (cTn I), α-hydroxybutyrate dehydrogenase (HBDH), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels in the serum, and ameliorate the pathological injury of AMI in rats. Metabolomics and network pharmacology of components absorbed in to plasma showed that PS may regulate the PI3K/Akt/NF-κB pathway and arachidonic acid metabolism, then ameliorate myocardial ischemic injury. This study found that PS significantly improved cardiac function in rats with AMI, through the PI3K/Akt/NF-κB pathway and arachidonic acid metabolism.

The pharmacokinetics (PK) of Rhodiola crenulata in rats were studied, and pharmacokinetic–pharmacodynamic (PK-PD) correlation analysis was performed to elucidate their time–concentration–effect relationship. The myocardial ischemia model was made with pituitrin. Rats were divided into sham operation, sham operation administration, model, and model administration groups (SG, SDG, MG, and MDG, respectively; n = 6). Blood was collected from the fundus venous plexus at different time points after oral administration. The HPLC-QQQ-MS/MS method was established for the quantification of five components of Rhodiola crenulata. CK, HBDH, SOD, LDH, and AST at different time points were detected via an automatic biochemical analyzer. DAS software was used to analyze PK parameters and PK-PD correlation. The myocardial ischemia model was established successfully. There were significant differences in the PK parameters (AUC0–t, AUC0–∞, Cmax) in MDG when compared with SDG. Two PD indicators, CK and HBDH, conforming to the sigmoid-Emax model, had high correlation with the five components, which indicated a delay in the pharmacological effect relative to the drug concentration in plasma. The difference in the PK parameters between modeled and normal rats was studied, and the time–concentration–effect of composition and effect indicators were investigated. This study can provide reference for the rational clinical application of Rhodiola crenulata and for related studies of other anti-myocardial ischemia drugs.

Introduction: Psoriasis is a chronic recurrent dermatological disease that patients always suffer from different comorbidities. Chinese herbal medicine has been commonly used in the treatment of psoriasis for a long history. However, the mechanism operating between Qing-Ying Dizhuo Decoction (QYDD) (a heat-clearing and blood -cooling decoction) and psoriasis remains unclear. This paper aimed to study the role of QYDD in psoriasis and its underlying mechanism.Methods: HaCaT cells were induced by a mixture of IL-22, IL-17A, oncostatin M, TNF-alpha and IL-1 alpha (M5) to construct the in vitro model of psoriasis. CCK-8 assay was utilized to assess the cell proliferation ability. The expressions of KRT1, KRT6, TNF-alpha, IL-1 beta, IL-6, IL-23, EZH2, I Kappa B alpha, p65 and IKK were determined by qRT-PCR, western blot and ELISA.Results: M5 induction increased levels of KRT6, IL-1 beta, IL-6, TNF-alpha and IL-23, enhanced the proliferation ability of HaCaT cells and decreased KRT1 expression, while QYDD treatment reversed these trends. Overexpression of EZH2 reversed the inhibitory effects of QYDD on cell inflammatory response and proliferation of M5-induced HaCaT cells. QYDD suppressed M5-activated NF-Kappa B signaling pathway as evidenced by decreased levels of phosphorylated IKK and p65 and increased level of phosphorylated I Kappa B alpha, while overexpression of EZH2 offset, in part, the regulation of the NF-Kappa B pathway by QYDD. An NF-Kappa B activator (betulinic acid) weakened the inhibitory effect of QYDD on the inflammatory response of HaCaT keratinocytes.Conclusion: QYDD appears to inactivate the NF-Kappa B signaling pathway by inhibiting EZH2, thereby repressing the proliferation and suppressing inflammatory response of HaCaT cells and attenuating psoriasis.

To investigate the mechanism underlying the effect of paeoniflorin (PF) on the proliferation and migration of psoriatic keratinocytes. The expressions of long noncoding RNA NEAT1, miR-3194-5p and Galectin-7 in skin tissues from psoriatic patients and healthy controls were detected. Psoriatic HaCat cells were used to investigate the function of NEAT1 and Galectin-7 as well as the effect and mechanism of PF in psoriasis. MTT, colony formation and scratch assays were used to assess the proliferation and migration of psoriatic HaCat cells. Dual-luciferase reporter assay was used to validate the interactions among NEAT1, miR-3194-5p and Galectin-7. NEAT1 and Galectin-7 were lowly expressed and miR-3194-5p was highly expressed in psoriatic patients. PF suppressed the proliferation and migration of psoriatic HaCat cells by elevating the expressions of NEAT1 and Galectin-7. NEAT1 positively mediated the expression of Galectin-7 by targeting miR-3194-5p. PF controls the proliferation and migration of psoriatic HaCat cells via the NEAT1/miR-3194-5p/Galectin-7 axis.

目的:从miRNA155-SOCS1轴调控Th17细胞及相关因子角度探索寻常型银屑病(PV)的发病机制,同时观察竹黄颗粒治疗PV的临床疗效及对miR-155、SOCS1和Th17细胞及相关因子的干预作用.方法:于竹黄颗粒治疗前后分别检测40例PV患者外周血PMBC中miR-155、SOCS1、RORγt、IL-17的mRNA表达水平及Th17细胞比例,血浆中IL-17、IL-6、IL-23的含量,随机选取15例同期体检健康者作为对照.并同时检测观察组中5例重度PV患者皮损与皮损周围组织中miR-155、SOCS1、RORγt及IL-17 mRNA的表达水平,以5例正常皮肤组织标本为对照.同时分析竹黄颗粒剂干预前后患者miR-155、SOCS1、RORγt及IL-17的基因表达及IL-17、IL-6、IL-23血浆含量的变化.结果:竹黄颗粒治疗后研究组总有效率达87.5％,PASI评分较治疗前明显降低(P<0.05).PV患者外周血PMBC中miR-155、RORγt、IL-17mRNA基因表达及Th17细胞比例较正常人显著上调,SOCS1下调(P<0.05),PV患者血浆中IL-17、IL-6和IL-23含量明显高于正常人(P<0.05),PV患者皮损组织、皮损周围组织及正常皮肤组织中miR-155,SOCS1、RORγt及IL-17mRNA基因表达水平差异有统计学意义(P<0.05),且皮损组织>皮损周围组织>健康正常皮肤组织,SOCS1反之.竹黄颗粒治疗后较治疗前miR-155、IL-17mRNA基因表达、Th17细胞比例及血浆IL-17水平显著下调,SOCS1上调(P<0.05).结论:miRNA155-SOCS1轴调控Th17细胞及相关因子与PV的发病有关,竹黄颗粒治疗血热型寻常型银屑病疗效显著,可能是通过调节miRNA155-SOCS1轴的表达、降低Th17细胞及相关因子水平发挥治疗作用.

AIMS: To investigate the cytoplasmic P21 expression regulating the apoptosis of human bronchial epithelial cell. MOTHEDS: The relationship of the cytoplasmic P21 expression with the apoptosis of 16HBE cells was studied after the plasmid pEGFP-N1-P21 was transfected into the 16HBE cells. After the 16HBE cells was the stimulated by the TGF-β1, the cytoplasmic and nucleic P21 expression and the apoptosis of 16HBE cell was detected, then the relationship of the P21 expression with the apoptosis of 16HBE cells was studied. RESULTS: The 16HBE cell had the basic low cytoplasmic and mainly high nucleic P21 protein expression, the plasmid PEGFP-N1-P21 could express P21 protein only in the cytoplasm of 16HBE cell and did not affect the nucleic P21 protein level. The apoptosis of 16HBE cells after transfection of the PEGFP-N1-P21 decreased. The apoptosis of 16HBE cells decreased as the time of the PEGFP-N1-P21 transfection increased, but the apoptosis of 16HBE cells increased without the PEGFP-N1-P21 transfection. The stimulation by TGF-β1 led to the expression of the cytoplasmic and nucleic P21 proteins, but mainly the cytoplasmic P21 protein expression, as the stimulation concentration of TGF-β1 increased, the cytoplasmic P21 expression decreased, but the nucleic P21 did not change. The apoptosis of 16HBE cells increased as the cytoplasmic P21 expression decreased after the concentration of TGF-β1 stimulation increased. CONCLUSIONS: The apoptosis of 16HBE cell was inhibited by the high cytoplasmic P21 expression through the transfection of PEGFP-N1-P21. TGF-β1 stimulation promoted the apoptosis of 16HBE cell by inhibiting the cytoplasmic P21 expression. The cytoplasmic P21 expression depresses the apoptosis of 16HBE cells.

Background: This study investigates the effect of epigallocatechin gallate (EGCG) from tea leaves on hyperuricemia and explores the underlying mechanisms in vitro and in vivo. Methods: The effects of EGCG on proliferation of BRL 3A rat liver cells were evaluated by CCK8 and after stimulation by xanthine the uric acid and xanthine oxidase (XOD) levels were evaluated by a kit; In an in vivo experiment, rats were treated with oxonic acid potassium salt combined with ethylamine pyrimidine to induce high uric acid hematic disease (7 days), The serum uric acid levels and XOD levels were evaluated by a kit, The expressions of OTA1 and GLUT9 were detected by RT-qPCR and Immunohistochemical. Results: EGCG had no effect on proliferation, and significantly reduced serum uric acid levels and inhibited XOD activity (P<0.05). The rat model exhibited a significant rise in blood uric acid levels (54.59 mg/dL), and EGCG significantly reduced the high level of serum uric acid and inhibited XOD activity in the serum and liver tissues (P<0.05). RT-PCR showed that EGCG significantly increased mOAT1 expression in the kidney tissues and reduced mGLUT9 expression (P<0.05). Immunohistochemical results showed that EGCG significantly increased OAT1 expression in the kidney tissues and decreased GLUT9 expression (P<0.05). Conclusions: These results demonstrate that EGCG has obvious anti-hyperuricemia effects in vitro and in vivo via the inhibition of XOD activity and GLUT9 expression and the promotion of OAT1 expression.

目的 研究细胞周期蛋白依赖性激酶抑制蛋白P21抑制人支气管上皮细胞凋亡的机制.方法 (1)表达细胞周期蛋白依赖性激酶抑制蛋白P21的质粒PEGFP-N1-p21转染人支气管上皮细胞系16HBE,研究P21蛋白在细胞质、细胞核内的表达变化与质粒转染后细胞凋亡表现之间的相互关系.实验分组包括空白对照、空质粒及PEGFP-N1-p21质粒组,应用Westen-blot方法检测质粒转染24 h后P21蛋白在细胞质、细胞核内的表达变化相对值,流式细胞仪方法检测质粒转染24 h、48 h后的细胞凋亡率.(2)转化生长因子-β1(TGF-β1)刺激人支气管上皮细胞系16HBE,研究TGF-β1刺激后P21蛋白在细胞质、细胞核内的表达变化与支气管上皮细胞凋亡之间的相互关系.实验分组包括TGF-β10 ng/mL、TGF-β13 ng/mL及TGF-β110 ng/mL组,应用Westen-blot方法检测TGF-β1刺激24 h后P21蛋白在细胞质、细胞核内的表达变化,流式细胞仪方法检测TGF-β1刺激12 h、24 h后的细胞凋亡率.结果 质粒PEGFP-N1-p21转染人支气管上皮细胞系16HBE 24 h后,PEGFP-N1-p21质粒组的P21蛋白在细胞质内表达水平高于空质粒组、空白对照组,并高于同组细胞核内,差异均有统计学意义(P<0.05);空质粒组、空白对照组的细胞质内P21蛋白表达水平低于细胞核内,差异均有统计学意义(P<0.05).PEGFP-N1-p21质粒转染24 h、48 h后,PEGFP-N1-p21质粒组凋亡率低于空质粒组及空白对照组,差异均有统计学意义(P<0.05).PEGFP-N1-p21质粒转染24 h后的16HBE细胞凋亡率高于转染48 h后,而空质粒组和空白对照组表现相反结果.PEGFP-N1-p21质粒转染后,P21蛋白在细胞质内表达与转染后的细胞凋亡呈负相关.TGF-β1(0 ng/mL、3 ng/mL、10 ng/mL)作用于16HBE细胞24 h后,TGF-β13 ng/mL及10 ng/mL组的细胞核、细胞质内P21蛋白表达均高于TGF-β10 ng/mL组,差异均具有统计学意义(P<0.05),TGF-β13 ng/mL及10 ng/mL组的细胞质中P21蛋白表达均高于细胞核内P21蛋白(P均<0.05),10 ng/mL组胞质P21蛋白表达量低于3 ng/mL组(P<0.05).TGF-β1(0 ng/mL、3 ng/mL、10 ng/mL)作用于16HBE细胞12h、24 h后,同一作用时间下,随着TGF-β1刺激浓度增加,细胞凋亡率增加,TGF-β1(3 ng/mL、10 ng/mL)作用于16HBE细胞12 h、24 h后,同一作用浓度下,随着刺激时间延长,细胞凋亡率增加(P均<0.05).TGF-β1作用于人支气管上皮细胞系16HBE后,细胞质内P21蛋白增加与刺激后的细胞凋亡呈负相关.结论 PEGFP-N1-p21质粒转染人支气管上皮细胞后,P21蛋白表达于细胞质,抑制人支气管上皮细胞凋亡.TGF-β1作用于人支气管上皮细胞系16HBE后,刺激细胞质内P21蛋白表达增加,随着细胞质内P21蛋白表达下降,细胞凋亡增加.细胞周期蛋白依赖性激酶抑制蛋白P21可通过在细胞质内高表达这一机制抑制人支气管上皮细胞凋亡.

目的 研究不同烟龄对健康人群细胞及体液免疫功能的影响.方法 纳入2014年1月至2016年12月在我院体检的400例男性健康体检者(排除任何急性及慢性疾病,尤其需要除外呼吸系统、心血管系统、风湿免疫系统、肿瘤、慢性肝炎等疾病),年龄45-60岁,根据吸烟指数分为:⑴非吸烟组:既往及目前均不吸烟者100例;⑵吸烟指数<300组(吸烟指数=吸烟年数×每天吸烟支数):100例;⑶吸烟指数300-400组:100例;⑷吸烟指数>400组:100例.4组患者均在清晨空腹抽取静脉血分别行T淋巴细胞亚群(CD3+％,CD4+％,CD8+％,CD4+/CD8+)及免疫球蛋白IgA、IgG、IgM的检测.结果 吸烟指数300-400组、吸烟指数>400组与非吸烟组相比,CD3+％、CD4+％均明显降低,差异具有统计学意义(P值<0.01).吸烟指数<300组与非吸烟组相比,T淋巴细胞亚群差异无统计学意义.3个吸烟组之间相比随着吸烟指数的增加CD3+％有下降趋势,差异有统计学意义.吸烟指数<300组、吸烟指数300-400组、吸烟指数>400组与非吸烟组相比,CD8+％,CD4+/CD8+,IgA、IgG、IgM差异均无统计学意义.结论 吸烟指数大于300可以损害人体的细胞免疫功能,表现为CD3+％、CD4+％的下降,且随着吸烟严重程度的提高,这种下降更明显.

Objective To determine the function and transcriptional regulatory elements of the regulatory region of-810~-769 bp upstream from the transcription initiation site of the human glutamate-cysteine ligase catalytic subunit (GCLC) gene. Methods The human GCLC gene regulatory region fragments were cloned and the wild-type plasmids were constructed. The mutant expression plasmids of deletion mutant-770~-766 GATAAG nucleotides and the site-directed mutant-765 and-764 GC to TA,-755 and-754 GG to TA were constructed. The transcriptional regulatory was determined by plasmid transfection. EMSA+super-shift method was used to identify transcriptional regulatory elements of-810~-769 bp upstream from the transcription initiation site of GCLC gene. Results The-810~-769 bp upstream of the transcription initiation site of human GCLC gene is the positive regulatory region,including NF-κB and AP-2 transcriptional elements. The transcription factor AP-2 could inhibit the binding of transcription factor NF-κB to the upstream-790~-766 DNA sequence of human GCLC gene transcription initiation site. Conclusion The regulatory region of-810~-769 bp upstream from the transcription initiation site of the human GCLC gene is a newly discovered positive regulatory region,which contains NF-κB and AP-2 regulatory elements.

喻文球运用阳和汤加减治疗中医外科疾病经验丰富,尤其是用治结节囊肿性痤疮、皮脂腺囊肿、寒冷性荨麻疹、乳腺炎和乳腺增生症,强调病虽不同,但须紧抓阳虚寒凝之病机,突出中医学“异病同治”观念,临床上取得满意疗效.

This paper introduces the clinical experience of applying'clear away heat and promote diuresis therapy'in seborrheic skin dis-eases by professor Yu Wen-qiu.Professor Yu Wenqiu pointed out that seborrheic skin diseases all have same pathological mechanism and clinical features of excess sebum secretion, sebum overflow and skin greasiness , with common pathogenesis:the spleen and stom-ach's failure in transformation cause disturbance in asending and decending and induce stasis of damp and heat.Damp and heat cause the lung's failure in both dispersing and decending causing blocking up of water passage and irregular opening and closing of the urinary bladder producing internal damp and heat.Heat cause oil secretion ang rising of water cause the floating up of oil.So excess sebum se-cret and overflow.Emphasizes the importance of damp-heat in the pathogenesis and establish 'clear away heat and promote diuresis therapy'of these diseases universally.This article also analyzes and summarizes the theory original of'clear away heat and promote diure-sis therapy'using by professor Yu Wen-qiu and clinical application feelings and experiences of diagnosis and treatment characteristics.

The purpose of this thesis is probing how to establish long-run effective mechanism through analyzing the features,new situations and problems of united front in universities.

Objective To discuss the influence of NPZBD on ability of learning and memory and bFGF positive neurons in Caudate putamen and cortex of aged hypomnesia rats.Methods The aged rats were randomly divided into normal memory group,hypomnesia group,NPZBD low dose treatment group and NPZBD large dose treatment group.The aged rats of treatment group were administered with NPZBD 0.05 g/(kg·d) and 0.1 g/(kg·d)for 15 d.All rats were tested ability of learning and memory with Morris water maze after the administration and detected the changes of bFGF Positive neurons in Caudate putamen and cortex with immunohistochemistry.Results In 4th to 5th day of splace navigation,the escape latency of rats in NPZBD large dose treatment group was significantly shorter than that of hypomnesia group,there was significant difference(P<0.05);in space probe test,the time in second quadrant,time of first through platform,times of through platform of rats in NPZBD large dose treatment group was significantly different with the rats in hypomnesia group(P<0.05).The bFGF positive neurons in Caudate putamen and cortex of aged hypomnesia rats in NPZBD large dose treatment group was significantly increased than those of hypomnesia group(P<0.05).Conclusion NPZBD has obvious promotion effect on ability of learning and memory in aged hypomnesia rats.The mechanism might be connected with increased bFGF positive neurons in Caudate putamen and cortex of aged hypomnesia rats.

Objective:To observe the clinical efficacy of Fufang sanhuang lotion for infant eczema and detect the functional mechanism.Methods:Put 50 infant eczema cases into two groups,one is experimental group(30 cases) and another one is contract group(20 cases),and then observe the change of skin injury,symptoms,EOS and IgE before and after treatmentResults:The clinical effective rate of experiment group is 93.33%,compared with the clinical effective rate of contract group(65.00%),it has obvious affection.And the reoccurrence rate,level of IgE and EOS of two groups after receiving treatment have distinguished difference(P0.05).Conclusion:Fufang sanhuang lotion can improve the clinical efficacy of infant eczema and shorten the treatment course,the possible mechanism may be related with the function of decreasing the level of EOS and IgE.

目的:观察舒血宁联合低分子肝素钙治疗不稳定性心绞痛的临床疗效和安全性。方法:将入选不稳定性心绞痛59例患者,随机分为对照组30例和治疗组29例,观察治疗前后每日心绞痛发作次数、常规12导联心电图ST-T段改善情况、血小板计数、凝血时间、凝血酶原时间、纤维蛋白原、冠心病事件发生情况和出血并发症等。结果:治疗组30例,治疗1周后,患者心绞痛发作次数显著减少,心电图的ST段改变明显改善,与对照组比较差异有统计学意义(P<0.01)。结论:舒血宁联合低分子肝素钙治疗不稳定性心绞痛安全有效。

患者,男,66岁.就诊日期:2007年7月8日.主诉:两小腿丘疹、瘙痒反复发作5年,加重2个月.病史:5年前无明显诱因出现两小腿丘疹、瘙痒,曾多次至外院就诊,结合组织病理诊断为结节性皮肤淀粉样变,治疗给予抗组胺剂口服,局部皮质类固醇软膏外涂(具体药物不详),只能暂时缓解症状,皮损未见好转.患者既往体健,形体瘦小.现症见两小腿胫前黄豆大小丘疹,密集成片,伴少许鳞屑,顶部角化,皮损表面肤色呈暗褐色,局部皮肤增厚,扪之粗糙坚实,剧烈瘙痒,全身无其他症状;舌质暗、苔薄白,舌边有瘀点,脉弦.皮损组织病理:苏木素伊红(HE)染色显示表皮萎缩变薄,表皮突变平,真皮全层及皮下组织有大片均一红染、团块状的淀粉样蛋白沉积,血管壁亦有淀粉样蛋白沉积;

1 临床资料 患者,女性,55岁.因"反复咳嗽、咳痰,喘息发作2年,加重2个月"于2007年6月8日入院.入院查体:神志清楚;口唇无发绀;双肺呼吸音粗糙,两上肺可闻轻度呼气相哮鸣音,未闻及湿性啰音;心界不大,心律规整,肝脾未触及,双下肢无水肿.血常规、尿常规、大便常规、血生化及免疫学检查未见异常.反复多次痰查结核菌阴性.PPD试验阴性.