ETHNOPHARMACOLOGICAL SIGNIFICANCE:Shuanglu tongnao formula (SLTNF) has been clinically proven to have significant efficacy in the treatment of Ischemic stroke (IS), and is a promising formula for IS treatment. Still, the underlying mechanism is not clear. Whether SLTNF ameliorates ischemic brain injury by reversing the pro-inflammatory microenvironment after IS is an interesting field of investigation. AIM OF THE STUDY:Based on the result of network pharmacology and single-cell RNA sequencing (scRNA-seq), whether SLTNF mitigates cerebral ischemia/reperfusion (I/R) injury by reversing the pro-inflammatory microenvironment was investigated in vivo for the first time. MATERIALS AND METHODS:The mice middle cerebral artery occlusion (MCAO) model was established to induce focal cerebral I/R. Subsequently, the remission effects of SLTNF treatment for cerebral I/R injury were evaluated in the MCAO model. scRNA-seq data was used to analyze the immune microenvironment after IS in mice. scRNA-seq and Network pharmacology were applied to predict the mechanism of the treatment of IS by SLTNF. Western blot (WB) and immunofluorescence techniques were employed to validate the potential mechanism. RESULTS:The experimental results demonstrated that SLTNF dosage-dependently attenuated the infarct volume, neurobehavioral, cell morphology and Nissl bodies damage, and inhibited the apoptosis in cerebral I/R mice. Moreover, scRNA-seq results revealed that the number of NK cells, neutrophils, monocytes, astrocytes and microglia significantly increased after IS. The cell-cell interactions dominated by microglia after IS, the cell-cell interactions between microglia and other immune cells significantly heightened. Furthermore, SLTNF promoted the transition of M1 microglia to M2 type, eventually reversing the pro-inflammatory microenvironment. Combined analysis of scRNA-seq and Network pharmacology results predicted that AGE-RAGE signaling pathway could involve in the regulation of microglia polarization by SLTNF. WB results revealed that SLTNF significantly inhibited the protein expression of CCND1, IL-1β and p-STAT3, which belong to crucial targets of SLTNF and AGE-RAGE signaling pathway. CONCLUSION:SLTNF attenuated cerebral I/R injury by reversing the pro-inflammatory microenvironment via the AGE-RAGE signaling pathway in mice.

目的 探讨壮药双路通脑方对缺血-再灌注(I/R)脑损伤大鼠神经元自噬和凋亡的影响及可能机制.方法 SD大鼠随机分为假手术组,模型对照组,小、中、大剂量双路通脑方组,大剂量双路通脑方+AMPK激活剂AICAR组,每组18只.按照分组给予不同的药物干预7 d后,采用线栓法制备大脑中动脉栓塞模型.再灌注24 h后,评估大鼠神经功能缺损的程度;2,3,5-三苯基氯化四氮唑(TTC)染色观察脑梗死体积;苏木精-伊红(HE)染色观察缺血半影区海马CA1区神经元形态学变化;TUNEL染色检测神经元凋亡;透射电子显微镜观察自噬小体的形成;免疫荧光(IF)染色检测微管相关蛋白1轻链3(LC-3)-Ⅱ的表达;Western blotting检测自噬标志基因Beclin-1、LC3A/B、p62及腺苷酸活化蛋白激酶(AMPK)、哺乳动物雷帕霉素靶蛋白(mTOR)、Unc-51样激酶1(ULK1)及其磷酸化蛋白的表达.结果 与假手术组比较,模型对照组神经功能缺损评分、脑梗死体积、神经元凋亡率、自噬小体数量、LC3-Ⅱ阳性表达、海马组织Beclin-1蛋白水平和LC3-II/LC3-I、p-AMPK/AMPK、p-ULK1(S317)/ULK1比值显著升高,p62蛋白水平和p-mTOR/mTOR、p-ULK1(S757)/ULK1比值显著降低(P<0.05);与模型对照组比较,小、中、大剂量双路通脑方组大鼠神经功能缺损评分、脑梗死体积、神经元凋亡率、自噬小体数量、LC3-Ⅱ阳性表达、海马组织Beclin-1蛋白水平和LC3-II/LC3-I、p-AMPK/AMPK、p-ULK1(S317)/ULK1比值显著降低,p62蛋白水平和p-mTOR/mTOR、p-ULK1(S757)/ULK1比值显著升高(P<0.05),且呈剂量依赖性;AICAR可明显减弱大剂量双路通脑方对脑I/R大鼠神经元自噬和凋亡的抑制作用.结论 双路通脑方可能通过调控AMPK/mTOR信号通路,抑制神经元的过度自噬,减少神经元凋亡,进而发挥对脑I/R大鼠的神经保护作用.

中医扶阳理论中元阳虚衰在中风发病过程起着重要的基础作用,阳化气不足,阴成形太过后,痰、瘀、毒等病理产物导致龙路堵塞,火路不通,进而形成缺血性中风.治疗方法为扶其元阳,使阴阳在其本位,在此基础上根据缺血性中风的病情使用三焦次第法中的开上焦、中焦,与壮医通"龙路、火路"有很大的内在逻辑相关性.故治疗应把握上、中焦温通的整体变化,以恢复"龙路、火路"为核心,并根据病理产物的动态变化采用健脾化湿、宣肺化痰、温肾助阳等治法,多脏同调,促使"龙路、火路"通畅,进而治愈本病.

目的 探讨壮宣饮对H1N1 流感病毒性肺炎大鼠肺损伤及TLR3/TAK1/NF-κB信号通路的影响.方法 将大鼠随机分为对照组、模型组、奥司他韦组(13.5 mg/kg)和壮宣饮高、中、低剂量组(14.0、7.0、3.5 g/kg),每组 12只.采用甲型流感病毒H1N1 滴鼻法建立流感病毒性肺炎大鼠模型,造模 24h后灌胃给予相应剂量药物.给药 5d后观察大鼠一般状态变化,检测大鼠支气管肺泡灌洗液(BALF)中TNF-α、IFN-γ、IL-6 水平,计算肺湿/干重比,HE染色观察大鼠肺组织病理学变化,RT-qPCR法检测肺组织H1N1 病毒载量,Western blot法检测肺组织TLR3/TAK1/NF-κB信号通路相关蛋白表达.结果 与对照组比较,模型组大鼠精神萎靡、毛色无光泽、呼吸加快、行动迟缓、体质量下降,肺湿/干重比值和BALF中TNF-α、IFN-γ、IL-6 水平升高(P<0.01),肺组织病理学评分、H1N1 病毒载量、TLR3、p-IκBα蛋白表达及 p-TAK1/TAK1、p-NF-κB p65/NF-κB p65 比值升高(P<0.01),IκBα 蛋白表达降低(P<0.01);与模型组比较,奥司他韦组和壮宣饮各剂量组大鼠精神状态良好,皮毛有光泽,呼吸较平稳,体质量增加,肺湿/干重比值和BALF中TNF-α、IFN-γ、IL-6 水平降低(P<0.05,P<0.01),肺组织病理学评分、H1N1 病毒载量、TLR3、p-IκBα蛋白表达及p-TAK1/TAK1、p-NF-κB p65/NF-κB p65 比值降低(P<0.05,P<0.01),IκBα蛋白表达升高(P<0.05,P<0.01).结论 壮宣饮可有效降低促炎细胞因子的释放,减轻H1N1 流感病毒性肺炎大鼠的肺损伤,其作用机制可能与抑制TLR3/TAK1/NF-κB信号通路有关.

目的:探讨艾司氯胺酮(Esket)调控miR-204-5p/趋化因子受体4(CXCR4)轴对机械通气诱导的大鼠肺损伤的影响.方法:将SD大鼠随机分为对照组(NC组)、模型组(model组)、低剂量Esket组(Esket-L组)、高剂量Esket组(Esket-H组)、an-tagomir阴性对照组(antagomir NC组)、miR-204-5p antagomir组、Esket-H+antagomir NC组、Esket-H+miR-204-5p antagomir组.除NC组外,其余各组大鼠机械通气4h,在机械通气前3d给予相应药物处理.比较各组肺组织湿重(W)/干重(D)比值、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量及血清中白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α)水平,苏木精—伊红(HE)染色观察大鼠肺组织病理变化,TUNEL法检测肺组织细胞凋亡率,实时荧光定量PCR(RT-qPCR)法检测miR-204-5p表达,western blotting法检测Bax、Caspase-3、CXCR4蛋白表达.结果:与model组比较,Esket-L组、Esket-H组肺组织病理损伤减轻,肺损伤评分、W/D比值、细胞凋亡率、MDA、IL-6、TNF-α、Bax、Caspase-3、CXCR4表达水平降低,SOD活性和miR-204-5p表达量升高(均P＜0.05).与model组、antagomir NC组比较,miR-204-5p antagomir组肺组织病理损伤加重,肺损伤评分、W/D比值、细胞凋亡率、MDA、IL-6、TNF-α、Bax、Caspase-3、CXCR4表达水平升高,SOD活性和miR-204-5p表达降低(均P＜0.05).miR-204-5p antagomir减弱了Esket-H对机械通气诱导的大鼠肺损伤的改善作用(P＜0.05).双荧光素酶报告基因实验证实miR-204-5p可靶向调控CXCR4表达(P＜0.05).结论:Esket可能通过上调miR-204-5p来抑制CXCR4表达,进而减轻机械通气诱导的大鼠肺损伤.

病毒性肺炎是一种基于病毒感染引发的肺实质、肺间质急性炎症疾病,患者基于病毒感染引发肺部损伤症状的同时亦有明显的炎症反应.中医药治疗病毒性肺炎有长久历史和丰富经验,可结合病毒性肺炎患者的实际情况选择中药汤剂、中成药等进行治疗,同时中药雾化吸入以及针灸、推拿、穴位贴敷等其他特色技术在病毒性肺炎的治疗中亦有良好的应用成效.本次研究即针对中医有关病毒性肺炎的认知进行总结,同时对中医药治疗病毒性肺炎的各种方法进行简单阐述.

BackgroundChildren with severe adenoviral pneumonia (ADVP) have poor prognosis and high risk of mortality. We performed a meta-analysis to evaluate the association between pretreatment lactate dehydrogenase (LDH) and severity, postinfectious bronchiolitis obliterans (PIBO), and mortality in children with ADVP.MethodsRelevant observational studies were identified by search of PubMed, Embase, Web of Science, Wanfang, and CNKI databases from inception to August 3, 2022. A random effect model was used to pool the results by incorporating the potential between-study heterogeneity.ResultsOverall, 23 studies with 4,481 children with ADVP were included in this meta-analysis. Results of meta-analysis showed that children with severe ADVP had a significantly higher level of pretreatment LDH as compared to those with non-severe ADVP (standard mean difference [SMD]: 0.51, 95% confidence interval [CI]: 0.36 to 0.66, p < 0.001; I2 = 69%). Besides, pooled results also suggested that the pretreatment LDH was significantly higher in children who developed PIBO as compared to those who did not (SMD: 0.47, 95% CI: 0.09 to 0.84, p = 0.02, I2 = 80%). Finally, results of the meta-analysis also confirmed that a higher pretreatment LDH (>500 IU/L) was a risk factor of increased mortality during hospitalization (odds ratio: 3.10, 95% CI: 1.62 to 5.92, p < 0.001, I2 = 0%). Sensitivity analyses by excluding one dataset at a time showed consistent results.ConclusionHigh pretreatment LDH may be associated with disease severity, development of PIBO, and increased risk of mortality in children with ADVP.

This study used a metabolomic approach to reveal changes in the levels of metabolic biomarkers and related metabolic pathways before and after Zhuang Yao Shuang Lu Tong Nao granule (YHT) treatment in rats with cerebral ischemia. The neurological deficit scores were significantly higher in the MCAO_R group than in the NC group, indicating that the mice had significantly impaired motor functions. The YHT group had significantly lower scores than the MCAO_R group, suggesting that YHT significantly improved motor function in rats. TTC staining of the brain tissue revealed that YHT significantly reduced the area of cerebral infarction in the treated rats. The MCAO_R group was better separated from the NC rent, sham, and YHT groups via metabolomic PCA. Moreover, there were significant differences in the differential metabolites between the MACO_R and YHT groups. Eighteen common differential metabolites were detected between the MACO_R and NC groups, MACO_R and sham groups, and MACO_R and YHT groups, indicating that YHT significantly increased the levels of various metabolites in the serum of cerebral ischemic stroke (CIS) rats. Moreover, a total of 23 metabolic pathways were obtained. We identified 11 metabolic pathways with the most significant effects in the bubble plots. In conclusion, from a systems biology perspective, this metabolomics-based study showed that YHT could be used to treat ischemic stroke by modulating changes in endogenous metabolites.

目的:研究日间光疗联合壮药浴治疗新生儿黄疸相比其他治疗方式的优点.方法:将确诊新生儿黄疸90例按随机数字表法分为对照1组、对照2组、观察组各30例.对照1组予住院光疗,对照2组予日间光疗,观察组予日间光疗,并在日间光疗结束后带壮药退黄方剂回家药浴,每天1次.对照2组及观察组日间光疗后连续3天早晨回门诊复测经皮胆红素值(TCB),如达光疗标准,继续予日间光疗.观察3组日均胆红素值下降幅度、光疗时间、治疗费用、不良反应、家长满意度,并评价临床疗效.结果:与对照1组、对照2组相比,观察组在治疗结束后TCB、日均胆红素值下降幅度、光疗时间、治疗费用及3天疗效差异均有统计学意义(P＜0.05);观察组患儿家长满意度与对照1组差异有统计学意义(P＜0.05),与对照2组差异无统计学意义(P＞0.05);对照1组与对照2组比较,治疗后TCB及日均胆红素值下降幅度差异无统计学意义(P＞0.05);对照1组有3例发生不良反应,观察组与对照2组均无不良反应病例.结论:日间光疗结合壮药浴治疗新生儿黄疸光疗时间短,不良反应少,经济实用,疗效显著,家长满意度高,可作为新生儿黄疸一种新的治疗方式.

Background: Ursolic acid (UA) is a pentacyclic triterpenoid compound with a wide range of anti-tumor, antiinflammatory, hypotensive and other pharmacological effects. Here, the biological roles and regulatory mechanisms of UA in influenza A virus (IAV)-treated A549 cells were investigated. Method: The cytotoxic impacts of UA on A549 cells with or without IAV treatment were determined using MTT and LDH assays. The inflammatory responses and oxidative stress of IAV-treated A549 cells were measured by RT-qPCR, ELISA, DCFH-DA probe, and colorimetric assays. A dual luciferase assay was carried out to validate the molecular interaction between miR-34c-5p and TLR5. Promoter methylation was detected by MSP experiment. Methylation-related proteins were quantified by western blot. Virus replication was assessed by TCID50 and western blot assays. Results: UA significantly ameliorated IAV-triggered cell injury and inflammatory response, virus replication and oxidative stress by elevating cell viability, ROS level and the activities of SOD and GSH-Px but reducing the LDH, MDA, and TCID50 values and the expression of virus-related proteins (NP) and cytokines (TNF-alpha, IL-1 beta, IL-6, and IL-18). Moreover, UA promoted miR-34c-5p expression by repressing DNMTs-mediated methylation. TLR5 was verified to be a direct target of miR-34c-5p and could be downregulated by UA. Rescue experiments revealed that silencing miR-34c-5p diminished the regulatory roles of UA in IAV-treated A549 cells. Conclusion: Our data elucidated that UA attenuated IAV-triggered inflammatory responses and oxidative stress in A549 cells by regulating the miR-34c-5p/TLR5 axis, suggesting that UA plays a protective role in IAV-induced pneumonia.

Pachymic acid (PA) plays a neuroprotective role during cerebral ischemia/reperfusion. However, the protective mechanisms of PA in cerebral ischemia/reperfusion have been not fully determined. This investigation aims to explore the neuroprotective role of PA in ischemia/reperfusion via miR‑155/NRF2/HO‑1 axis. The N2a cell line was induced by hypoxia/reoxygenation (H/R) to simulate the neuronal damage that occurs during cerebral ischemia/reperfusion. PA was used to treat H/R‑induced N2a cells. An MTT assay was used to determine cell viability. The protein levels of Bcl‑2, Bax, heme oxygenase‑1 (HO‑1) and nuclear factor E2‑related factor 2 (NRF2) were measured via Western blot analysis. The level of apoptosis of N2a cells was determined by flow cytometry. The expression levels of miR‑155 and NRF2 were quantified by real‑ti me PCR. PA treatment inhibits the increase in apoptosis induced by H/R and also enhances the viability of cells exposed to H/R. PA reverses the increased expression of miR‑155 caused by H/R. Furthermore, H/R does not change the expression of HO‑1 and NRF2, but PA upregulates the expressions of HO‑1 and NRF2. Additionally, NRF2 is the target of miR‑155. Inhibiting miR‑155 contributes to increased cell viability and decreased apoptosis via targeting the NRF2/HO‑1 pathway. Overall, PA prevents neuronal cell damage induced by hypoxia/reoxygenation via miR‑155/ NRF2/HO‑1 axis.

目的:系统评价以温阳为主要功效的中药复方对血管性痴呆(VaD)的临床疗效.方法:检索VIP、CNKI、CBM、WanFang Data、PubMed等数据库,手工检索《中国中西医结合杂志》(英文版)、《中医杂志》(英文版)中关于温阳为主要功效的中药复方治疗血管性痴呆的文献,对检索文献进行Meta分析.结果:最终纳入文献11篇,均是中文文献,共790例受试对象.Meta分析结果显示:当治疗疗程≥12周,与对照组比较,以温阳为主要功效的中药复方在改善MMSE评分(MD=3.70,95％CI[1.06,6.34],P=0.006),ADL评分(SMD=-0.49,95％CI[-0.82,-0.15],P=0.004)、HDS评分(MD=3.68,95％CI[1.77,5.60],P=0.0002)、中医证候评分(OR=10.09,95％CI[2.78,36.63],P=0.0004)、临床总有效率(OR=4.36,95％CI[2.35,8.08],P<0.00001)方面效果更好.结论:以温阳为主要功效的中药复方在改善血管性痴呆患者MMSE、ADL、HDS评分、中医证候以及临床总有效率方面优于现有西医治疗或其他对症治疗,且现有的证据资料未发现明显毒副作用.

AbstractThe specific mechanism of gingerol in cerebral ischemia remains unknown. A neuroprotective function for miR‐210 in cerebral ischemia has been identified. The brain‐derived neurotrophic factor (BDNF)‐mediated signaling pathway protects against cerebral ischemic injury. This investigation aimed to determine whether gingerol plays a neuroprotective role in cerebral ischemia via the miR‐210/BDNF axis. N2a cells subjected to 10 h of hypoxia and 4 h of reoxygenation were treated with 5, 10, or 20 μmol/L gingerol. The levels of viability, apoptosis, and proteins in N2a cells were determined using MTT assays, flow cytometry, and western blotting, respectively. The binding relationship between BDNF and miR‐210 was studied using a dual luciferase reporter assay. The expression levels of miR‐210 and BDNF were determined using qPCR. Gingerol repressed the increase in apoptosis and decrease in viability observed in response to hypoxia/reoxygenation. Gingerol increased Bcl‐2, BDNF, and TrkB levels and reduced Bax and cleaved caspase 3 levels after hypoxia/reoxygenation. Gingerol evoked decreased expression of miR‐210. Inhibition of miR‐210 resulted in increased viability and reduced apoptosis along with increased levels of Bcl‐2, BDNF, and TrkB and reduced levels of Bax and cleaved caspase 3 after hypoxia/reoxygenation. Additionally, the miR‐210 mimic reversed changes induced by gingerol. The cotransfection of the miR‐210 mimic and wild type BDNF led to decreased luciferase activity. BDNF was negatively regulated by miR‐210. BDNF siRNA reversed these changes evoked by miR‐210 inhibition. Gingerol ameliorated hypoxia/reoxygenation‐stimulated neuronal damage by regulating the miR‐210/BDNF axis, indicating that gingerol is worthy of further application in cerebral ischemia therapy.

目的 探讨中药浴辅助方法对不同病因新生儿高胆红素血症的疗效.方法 选取2018年9月至2020年10月我院新生儿高胆红素血症住院患儿322例,按不同病因随机分为观察组与对照组各161例.对照组采用蓝光照射,观察组在对照组治疗基础上采用中药浴.观察治疗前、治疗后48 h及结束时检测血清总胆红素值(TSB)变化,日均大便次数,光疗时间及疗效.结果 两组日均大便次数有明显差异(P＜0.05),光疗时间无明显差异(P＞0.05),短期疗效无明显差异(P＞0.05).两组治疗结束后TSB在母乳性黄疸有统计学意义(P＜0.05).观察组随着治疗时间的延长,不同病因TSB下降的幅度不同(P＜0.05).治疗后48 h G-6-PD缺乏病因与其他病因比较有差异性(P＜0.05),治疗结束时G-6-PD缺乏病因与母乳性黄疸及围产期高危因素比较有差异性(P＜0.05).结论 应用本法中药浴辅助治疗新生儿高胆红素血症与单纯西医蓝光照射短期疗效相同.但中药浴辅助治疗对母乳性黄疸更有效,而对G-6-PD缺乏症黄疸的疗效相对低于其他病因.

目的:观察扶阳方治疗缺血性中风(IS)恢复期阳虚证的临床疗效,并探讨其作用机制.方法:将50例IS恢复期阳虚证患者随机分为治疗组和对照组,每组各25例.2组均予以基础治疗,在此基础上治疗组加用扶阳方治疗,对照组加用补阳还五汤治疗,2组均治疗28 d.观察2组治疗前、治疗14 d后、治疗28 d后日常生活活动能力(ADL)评分、美国国立卫生研究院卒中量表(NIHSS)评分、生活质量评分、中医证候积分及安全性,并评价临床疗效.结果:总有效率治疗组为92.00％(23/25),对照组为76.00％(19/25),2组比较,差异有统计学意义(P＜0.05);2组ADL评分、NIHSS评分、生活质量评分、中医证候积分治疗前后组内比较及治疗后同时间节点组间比较,差异均有统计学意义(P＜0.05或P＜0.01);2组治疗前后血常规、大便常规、尿常规及肝肾功能均未出现明显改变.结论:扶阳方治疗IS恢复期阳虚证疗效确切,明显优于补阳还五汤,为运用中医扶阳理论治疗IS恢复期提供了临床证据.

目的:观察红鞭岗梅汤治疗风热乘脾型疱疹性咽峡炎的临床疗效.方法:将风热乘脾型疱疹性咽峡炎患儿80例按照随机数字表法分为观察组(红鞭岗梅汤)和对照组(蒲地蓝消炎口服液)各40例,疗程5天.回顾性分析两组患儿治疗前后疱疹消退时间、体温降至正常时间、进食量恢复时间、流涎恢复时间以及各证候积分变化情况,观察两组患儿用药安全性、依从性及不良事件发生情况.结果:治疗后两组患儿咽峡部疱疹积分比较差异有统计学意义(P<0.05),发热、食欲、流涎积分两组比较差异无统计学意义(P>0.05),在退热、进食量恢复及流涎消失时间方面两组比较差异无统计学意义(P>0.05).总有效率观察组为95％,对照组为84.6％,两组比较差异无统计学意义(P>0.05).观察组服药依从性为100％,对照组76.9％,差异有统计学意义(P<0.05);不良反应发生率观察组为0％(0/40),对照组为7.7％(3/39),两组比较差异无统计学意义(P>0.05).结论:红鞭岗梅汤可减轻风热乘脾型患儿的咽峡部疱疹,缩短其消失时间,提高患儿服药依从性,安全性与蒲地蓝消炎口服液相当.

目的 探讨抗复感颗粒对肺炎幼龄大鼠的干预作用及机制.方法 将50只大鼠随机分为正常组、模型组、头孢曲松组、抗复感颗粒组、抗复感颗粒加头孢曲松联合用药(简称联合用药)组,每组10只.运用肺炎链球菌经气管滴注构建制备幼龄大鼠肺炎模型.抗复感颗粒组给予209/(kg·d)抗复感颗粒灌胃及0.05 mL生理盐水肌肉注射;联合用药组给予抗复感颗粒20g/(kg·d)灌胃及肌肉注射头孢曲松100 mg/(kg·d);头孢曲松组给予0.6 mL/d生理盐水灌胃及肌肉注射头孢曲松100 mg/(kg·d);正常组、模型组均给予等量生理盐水灌胃及肌肉注射.连续给药5天后,观察大鼠一般情况;瑞氏-姬姆萨染色对肺泡灌洗液(BALF)中细胞的总数及分类细胞数计数;HE染色观察肺及大肠组织炎症细胞浸润;qRT-PCR法检测大鼠肺组织中肿瘤坏死因子(TNF-α)、IL-6 mRNA表达水平;系列生化法检测大鼠大便肠球菌、双歧杆菌、大肠杆菌、乳酸杆菌的变化.结果 与模型组比较,各药物干预组肺组织炎症细胞浸润明显改善;抗复感颗粒组肠道轻度炎症细胞浸润,联合用药组肠道无明显异常.与正常组比较,模型组大鼠体重减轻(P＜0.05),白细胞总数升高,其中中性粒细胞和淋巴细胞所占比例均升高(P＜0.01),巨噬细胞比例降低(P＜0.01);肺组织TNF-α、IL-6 mRNA水平升高(P＜0.01);肠道中肠球菌、大肠杆菌数增高,乳酸杆菌降低(P＜0.01).与模型组比较,各药物干预组白细胞总数、中性粒细胞及淋巴细胞比例均降低,巨噬细胞比例增高(P＜0.01),TNF-α、IL-6 mRNA水平降低(P＜0.01);抗复感颗粒组、联合用药组大鼠体重增加,肠道中肠球菌、大肠杆菌数降低,乳酸杆菌增多(P＜0.05,P＜0.01).联合用药组较头孢曲松组及抗复感颗粒组白细胞总数下降(P＜0.01),联合用药组较抗复感颗粒组乳酸杆菌减少(P＜0.01).结论 抗复感颗粒可改善肺炎幼龄大鼠肺组织炎症,降低肺组织炎性细胞因子IL-6、TNF-αmRNA水平,且不引起肠道微生态的紊乱.

目的:观察壮药龙盘止咳方对急性气管-支气管炎幼鼠模型IL-4/IFN-γ和基质金属蛋白酶的影响.方法:将Wistar幼鼠随机分成对照组、模型组,低、中、高剂量组和阳性治疗组.用烟熏法建立急性气管-支气管炎幼鼠模型,并采用不同剂量的壮药龙盘止咳方灌胃或小儿宣肺止咳颗粒治疗.治疗1周后取幼鼠血清及肺组织,采用ELISA法检测血清白介素-4(IL-4)和干扰素-γ(INF-γ)含量,采用qPCR和Western blot测定基质金属蛋白酶9(MMP-9)和金属蛋白酶组织抑制因子1(TIMP-1)含量.结果:与对照组比较,模型组幼鼠体质量较轻(P<0.05),经过壮药龙盘止咳方和小儿宣肺止咳颗粒治疗后的幼鼠体质量较模型组增加(P<0.05),低、中、高剂量组和阳性治疗组之间幼鼠体质量比较差异无统计学意义(P>0.05).与对照组比较,模型组幼鼠IL-4和MMP-9升高,IFN-γ和TIMP-1降低(P<0.05);与模型组比较,低、中、高剂量组和阳性治疗组幼鼠IL-4和MMP-9降低,IFN-γ和TIMP-1升高(P<0.05);与阳性治疗组比较,低、中低剂量组幼鼠各项指标无明显变化(P>0.05),高剂量组幼鼠IL-4和MMP-9降低,IFN-γ和TIMP-1升高(P<0.05);随着壮药龙盘止咳方剂量的增加,幼鼠IL-4和MMP-9降低,IFN-γ和TIMP-1升高(P<0.05).结论:壮药龙盘止咳方可逆转烟熏引起的急性气管-支气管炎模型IL-4升高和IFN-γ减少,增加TIMP-1表达、降低MMP-9表达,调节MMP-9/TIMP-1两者表达失衡,减轻急性气管-支气管炎.

目的 探讨龙盘止咳方治疗小儿咳嗽3个证型的临床疗效.方法 选择90例小儿咳嗽患儿(风热犯肺证、痰湿蕴肺证、痰热壅肺证病例各30例).各组均给予龙盘止咳方,每日1剂,5d为1个疗程.观察3组证型治疗前后临床疗效及中医证候评分等相关指标.结果 风热犯肺证、痰湿蕴肺证、痰热壅肺证的总有效率分别为89.66％、58.62％、75.86％;证候疗效,风热犯肺证＞痰热壅肺证＞痰湿蕴肺证(P＜0.05);单项症状积分,3组在咳嗽、咳痰、鼻塞、肺部哕音单项症状方面治疗前后差异有统计学意义(P＜0.05);流涕、咽充血、扁桃体方面治疗前后无显著差异(P＞0.05);3组不同证型患者在治疗前后中医证候积分下降程度不同(P＜0.01).结论 龙盘止咳方治疗小儿咳嗽的3个证型均有疗效,以风热犯肺证疗效更显著,且用药安全.

目的:通过星点设计-效应面法优选壮药盘龙止咳颗粒的最佳提取工艺,为后续研发更有效、更稳定、更方便的新制剂提供依据.方法:采用高效液相色谱法进行含量测定,采用单因素试验、星点设计-效应面法考察乙醇浓度、溶剂倍量、提取时间及提取次数,以山奈酚-3-0-龙胆二糖苷与岩白菜素总含量及干膏率的综合评分为评价指标,优选出壮药盘龙止咳颗粒最佳提取参数.结果:壮药盘龙止咳颗粒的最佳提取工艺为加入12倍量浓度为50％的乙醇,每次提取50 min,提取2次.结论:通过星点设计-效应面法优选盘龙止咳颗粒的提取工艺,方法预测性良好,重复性良好,简便可靠,为改变服用剂型研究提供了可靠依据.