BACKGROUND:Ulcerative colitis (UC) is a chronic inflammatory bowel disease with limited treatment options. The carbonization of Rubia cordifolia L. traditionally enhances its therapeutic effects, but the mechanism remains unclear. OBJECTIVE:To investigate whether carbonization induces self‑assembled nanoparticles (PRCL NPs) from Rubia cordifolia and to elucidate their mechanism in UC. STUDY DESIGN:Self‑assembled nanoparticles were extracted from raw (RCL NPs) and carbonized (PRCL NPs) Rubia cordifolia. A DSS‑induced acute UC mouse model was used to evaluate efficacy. Transcriptomics, proteomics, Western blot, and ELISA were performed to explore the mechanism. METHODS:Nanoparticles were characterized by DLS, SEM, FTIR, and stability assays. DSS‑induced colitis mice were orally treated with RCL NPs or PRCL NPs (1.3 and 5.2 g/kg). Inflammatory and pathway markers were assessed. RESULTS:PRCL NPs exhibited smaller particle size (337.2 nm vs. 947.2 nm) and enhanced stability (zeta potential -15.2 mV). Multi‑omics revealed convergent enrichment of the IL‑17 signaling pathway. PRCL NPs significantly upregulated IL‑17A, IL‑22, p‑STAT3, and p‑C/EBPβ (p < 0.001) and suppressed chemokines CCL5, CXCL5, and CXCL10. CONCLUSION:Carbonization of Rubia cordifolia spontaneously forms structurally optimized self‑assembled nanoparticles (PRCL NPs) that alleviate UC by modulating the IL‑17A/IL‑22-C/EBPβ-STAT3 axis. This study provides a modern nanoscale interpretation of traditional processing theory.

Background: Huangqin decoction (HQD), a classic formula for treating ulcerative colitis (UC), exhibits anti-inflammatory and intestinal mucosa protective effects. However, its mechanisms require further investigation. This study aimed to elucidate these mechanisms by integrating metabolomics and serum pharmacochemistry-based network pharmacology. Methods: A dextran sulfate sodium (DSS)-induced mice model of UC was established to assess the therapeutic effect of HQD. Chemical compounds and absorbed constituents of HQD were identified by UHPLC-Q-Orbitrap-MS. Network pharmacology predicted targets and pathways based on blood-absorbed constituents. Differential metabolites and associated pathways were identified by serum metabolomics. Fe2+ and GSH levels in colon tissues were measured to assess ferroptosis. Molecular docking evaluated binding affinities, and the expression of ferroptosis-related targets was validated by RT-qPCR and Western blot. Results: A total of 92 chemical compounds and 66 blood-absorbed constituents were identified. Compared to the DSS group, 44 differential metabolites were reversed in the HQD group, enriched in tryptophan metabolism, arginine and proline metabolism, and pyrimidine metabolism. Joint analysis of network pharmacology and metabolomics focused on the arachidonic acid pathway and ferroptosis-related targets. HQD inhibited ferroptosis, evidenced by decreased Fe2+ levels and restored GSH content. RT-qPCR, Western blotting, and molecular docking demonstrated that HQD bioactive components exhibited significant binding affinity for and regulatory activity toward four key ferroptosis-related targets: PTGS2, ALOX5, GPX4, and STAT3. Conclusion: The integrated analysis strategy suggests that the efficacy of HQD against UC may be associated with its regulation of inflammatory responses and ferroptosis-related targets, providing a preliminary basis for elucidating the material basis and mechanisms of HQD.

Aloe vera is a perennial herbaceous plant belonging to the lily family, and is widely utilised in traditional Chinese medicine and the beauty industry throughout the world. The primary active components extracted from this genus are polysaccharides, which have demonstrated significant pharmacological activities both in vivo and in vitro. This paper reviews the methods for the extraction, isolation, and purification of Aloe vera polysaccharides, along with their physicochemical properties and structural characteristics. Furthermore, the immunomodulatory, antioxidant, anti-inflammatory, anticancer, hypoglycemic, antibacterial, and other biological activities of Aloe vera polysaccharides are examined. Finally, the paper discusses quality control measures for Aloe vera polysaccharides, aiming to provide a reference for their development and utilization. This review serves as a resource for further research on the application of Aloe vera polysaccharides in food, dentistry, and orthopedics.

Background The global incidence of non-alcoholic fatty liver disease (NAFLD) is rising due to changes in modern lifestyle and dietary habits, making it one of the leading causes of chronic liver disease. NAFLD can progress to more severe liver conditions, imposing significant economic burdens. Currently, no FDA-approved drugs are available for its treatment. However, Traditional Chinese Medicine (TCM) has gained attention for its unique theoretical framework and therapeutic strategies, particularly its potential to improve liver health by modulating liver function. Recent studies have also highlighted TCM's ability to regulate gut microbiota, offering a promising avenue for NAFLD management. To better understand the evolving role of TCM in treating NAFLD, a comprehensive analysis of existing research is necessary. Methods In this study, the Web of Science database was chosen as the primary data source to investigate the treatment of non-alcoholic fatty liver disease (NAFLD) using traditional Chinese medicine (TCM). Specifically, the search focused on English articles and review articles indexed in the SCI-E and SSCI databases, spanning from January 1, 2012, to October 30, 2024. The search strategy employed the following formula: TS = (“non-alcoholic fatty liver disease” OR “Metabolic dysfunction-associated fatty liver disease” OR “NAFLD”) AND TS = (“TCM” OR “Herbal medicines”). The analysis encompassed various aspects such as authors, keywords, journals, countries, institutions, and references. For this purpose, analytical tools including VOSviewer, Bibliometrix, and CiteSpace were utilized to systematically evaluate the gathered data. Results A total of 306 documents were retrieved, indicating a rising trend in the number of publications, which is expected to accelerate in the future. China is at the forefront in terms of both the quantity of publications and total citations, demonstrating strong international collaboration. Within China, Shanghai University of TCM and Chengdu University of TCM are leading institutions, having established a stable group of collaborating authors. The top 10 key journals account for 49.02% of the publications, with Frontiers in Pharmacology being the most prolific, while the World Journal of Gastroenterology boasts the highest average number of citations. The most frequently cited journals are Hepatology, Journal of Hepatology, and Journal of Ethnopharmacology. Keyword analysis reveals that high-frequency terms such as steatohepatitis are prevalent, addressing topics like pathogenesis, indirect therapeutic effects, and molecular biological mechanisms. Recent outbreak word analysis highlights 'cell' and 'steatohepatitis' as current hotspots, with 'NASH' anticipated to be a focal point in 2024. Discussion The number of publications on TCM treatments for NAFLD has steadily increased, with TCM exhibiting therapeutic effects through various mechanisms, including anti-inflammatory, antioxidant, lipid metabolism modulation, and gut microbiota regulation. The anti-inflammatory effects primarily result from the inhibition of inflammatory signaling pathways. Antioxidant properties arise from bioactive compounds in TCM and their modulation of related pathways. Lipid metabolism improvement occurs through the regulation of spleen and stomach functions, promoting lipolysis. Furthermore, TCM regulates intestinal microbiota, restoring microbial balance and enhancing intestinal barrier function. Future research should focus on the synergistic mechanisms underlying these multiple pathways to develop more comprehensive therapeutic strategies. Additionally, expanding the data sources for further analysis is crucial. However, this study has limitations, including reliance on a limited selection of databases and keywords from Web of Science, which may not capture all relevant literature, and the potential bias in the bibliometric analysis.

Background:Arisaema cum bile (known as DanNan Xing in Chinese, DNX) is a traditional herbal medicine commonly used to treat febrile seizure (FS), but the underlying mechanism remains unclear. Objective:To evaluate the therapeutic effect of DNX on hot water bath-induced FS rat model and further explore the potential mechanism. Methods:The chemical constituents of DNX were determined via liquid chromatography-mass spectrometry (LC-MS). FS rat model was established using a hot water bath (45 ± 2 °C), and DNX (2.8 and 0.7 g/kg, i.g) were administered for two weeks. Based on behavior test (duration and latency), pathological changes in the hippocampal tissue, and the levels of inflammatory cytokines the therapeutic effect of DNX for FS was evaluated. Subsequently, the network pharmacology, 16S rRNA and non-targeted metabolomics analysis were combined analysis to explore the potential signaling pathway. Furthermore, the signaling pathway was verified using the RT-qPCR and immunohistochemistry assay. Results:The DNX treatment showed effective therapy on hot water bath induced FS, as indicated by a shortened seizure duration time, prolonged seizure latency, reduced hippocampal neuron damage and neuroinflammatory factor levels (TNF-α, IL-1β, IL-6, and HMGB1). Neurotransmitters (GABA, Glu) are also significantly regulated. Moreover, the relative abundance of Lactobacillus and Lachnospiraceae was notably increased (p < 0.01), while that of Tenericutes decreased, compared to gut microbiota of FS rat. A total of 20 fecal differential metabolites were regarded as the potential biomarkers including GABA, CDCA, and UDCA for anti-FS of DNX, and combined network pharmacy the metabolic pathways of primary bile acids (BAs) biosynthesis and alanine, aspartate and glutamate metabolism were involved. Conclusion:DNX possesses a therapeutic effect on FS through inhibiting neuroinflammation and regulation of FXR and GABA signaling pathway.

AIM OF THE STUDY:This paper reviews the progress of research on the botany, traditional uses, phytochemistry, pharmacology, modern uses and toxicity of Jasminum sambac (L.) Aiton (JS). MATERIALS AND METHODS:Literature for this paper on JS was obtained from databases such as Web of Science, PubMed, ACS Publications, Google Scholar, Baidu Scholar, and CNKI. Find botanical related information at The Catalogue of Life, Flora of China database. All chemical structures were drawn using Chemdraw23 software. RESULTS:JS is an erect or climbing shrub that grows mainly in tropical and warm temperate regions of South Asia, Southeast Asia, Europe, and Africa, and has been used in traditional medicine for the treatment of insomnia, headaches, dental caries, bruises, diarrhea and abdominal pain, dizziness and headaches, and difficult labor. More than 200 phytochemicals have been isolated and identified from JS, most of which are terpenes, aromatic compounds, organic acids and their derivatives. JS can be used in the development of antimicrobials, antioxidants, and cardiotonic agents; It has certain anti-inflammatory activity and anti-cancer activity; it also enhances immunity, vasodilates blood vessels and is anti-aging. In addition, JS has applications in the fields of ecological regulation, insecticide and food safety and security. CONCLUSION:In view of its long history of traditional applications, rich phytochemical composition, diverse pharmacological activities and modern application development, JS can be regarded as an important botanical resource in the field of traditional medicine as well as in the modern ecological and food fields. However, the current extraction methods and the limitations of JS itself, most of the studies on JS volatile compounds focus on volatile components, and the resulting components are not strictly screened, and lack of research on the characteristic components; In addition, although JS has a wealth of pharmacological effects, the contemporary research in the field of medicine is not enough to pay attention to its pharmacological aspects of the research has only been carried out preliminary cellular experiments and simple animal experiments, to exert the effect of the mechanism of action of the medicinal effect is not thoroughly researched. It is recommended to strengthen the research in the field of JS medicinal use, develop new dosage forms, and establish a special base for cultivation, planting and research of medicinal JS, so as to better realize the development and utilization of JS resources.

Non-alcoholic fatty liver disease (NAFLD) has been considered a main health concern worldwide, and Platycodon grandiflorum (PG) has been traditionally employed in ethnopharmacology for managing hepatic metabolic disorders. This study aimed to elucidate the potential effect of PG on NAFLD in rats, and furthermore, the mechanism was explored. PG supplementation significantly increased body weight, serum total cholesterol, triglycerides, and LDL-cholesterol levels in HFD-induced obese rats (p < 0.05). In addition, HFD-induced lipid accumulation and inflammatory response in the liver were also suppressed. Then, the factors contributing to the regulating effect of PG on NAFLD were estimated by using network pharmacology and RNA sequencing. Moreover, western blotting and reverse transcription quantitative polymerase chain reaction (RT-qPCR) suggested that PG treatment obviously downregulated the expression levels of nuclear factor-κB (NF-κB), Toll-like receptor 4 (TLR4), myeloid differentiation primary response protein 88 (MyD88), and inhibitor I kappa B alpha (IκBα), whereas it upregulated the expression of peroxisome proliferator-activated receptor-gamma (PPARγ). Taken together, these findings corroborated the modulatory capacity of PG on NAFLD rats through regulating inflammatory response via PPARγ and TLR4/NF-κB pathway.

BackgroundHyperlipidemia (HLP) presents a significant challenge to global public health. Mounting evidence suggests that statins, the recommended first-line lipid-lowering agents, have significant adverse effects. Consequently, the quest for natural and efficacious alternative therapies is steadily emerging as a research priority for HLP prevention and treatment. Consumption of tea, which is rich in diverse biologically active compounds with the capacity to regulate lipid metabolism and combat obesity, has emerged as a promising alternative therapy. Sea buckthorn leaves are rich in a multitude of biologically active substances, have a hypolipidemic effect, and can be used as a raw material for tea because of their unique flavor. There is a suggestion that combining Aspergillus cristatus with tea could modify or boost the lipid-lowering active compounds present in tea, thereby increasing its efficacy in regulating lipid metabolism.ResultsSea Buckthorn Leaf Fu Tea (SBLFT) was obtained by fermentation when sea buckthorn leaves contained 42% moisture, inoculated with Aspergillus cristatus 0.2 mL/g, and incubated for 8 d at constant temperature. Animal experiments demonstrated that SBLFT significantly inhibited body weight gain in HLP rats and reduced lipid content and serum oxidative stress. In addition, liver tissue sections and functional indices showed that SBLFT can improve liver morphology and function abnormalities. Reverse transcription-polymerase chain reaction results indicated that the expression of Liver kinase B1(LKB1), adenosine 5‘-monophosphate (AMP)-activated protein kinase(AMPK), acetyl CoA carboxylase1(ACC1), and sterol-regulatory element binding protein-1 (SREBP1c) gene related to lipid metabolism was altered.CONCLUSIONSBLFT improved HLP, specifically via promoting the expression of LKB1 in the liver of HLP rats, activating AMPK, and inhibiting ACC1 and SREBP1c expression, resulting in the inhibition of fatty acid and triglyceride synthesis-related enzymes at the transcriptional level.

Memory disorder (MD) is a neurodegenerative disease with an increasing incidence rate that adversely affects the quality of life of patients. Qifu Yin (QFY), a classic traditional Chinese medicine formula used for treating dementia, is known for its neuroprotective properties, although its mechanism of action requires further exploration. In this study, D-galactose combined with aluminum chloride was used to establish an MD rat model, and behavior, histopathology, and related indicators were used to evaluate the pharmacodynamics of the formula in the rats. Furthermore, brain tissues were examined using pseudo-targeted lipidomics analysis, and candidate ion pairs were screened through mass spectrometry using UPLC-Q/Orbitrap HRMS. An sMRM detection method for candidate ion pairs was developed using UHPLC-Q-TRAP-MS/MS and validated. This approach was applied to the lipidomics study of QFY in improving MD. Differential metabolites screened through pseudo-targeted lipidomics were analyzed by employing network pharmacology, and the pathway was verified to explore their mechanism of action. Results demonstrated that QFY could improve memory impairment. A total of 1052 ion pairs were constructed in the pseudo-targeted lipidomics analysis, identifying 33 differential metabolites and 5 metabolic pathways. Furthermore, 31 differential metabolites in MD rats treated with QFY were significantly reversed. Immunohistochemical analysis showed that QFY could inhibit the expression of inflammatory factors. Network pharmacological analysis showed that the calcium signaling pathway was the main signaling pathway, and QFY could significantly reverse the expression levels of mRNA and protein. Thus, QFY can improve memory impairment in rats, which may be related to the regulation of oxidative stress, lipid metabolism disorder and the calcium signaling pathway.

Percutaneous coronary intervention (PCI) is the main treatment for patients with severe coronary vascular stenosis. However, In-stent neo-atherosclerosis (ISNA) is an important clinical complication in patients after PCI, which is mainly caused by a persistent inflammatory response and endothelial insufficiency. In the cardiovascular field, magnesium-based scaffolds stand out due to their properties. Magnesium plays a key role in regulating cardiovascular physiology. Magnesium deficiency can promote endothelial cell dysfunction, which contributes to the formation of atherosclerosis. Since astragaloside IV (AS‑IV) has been proven to have potent cardioprotective effects, we asked whether high levels of magnesium cooperate with AS‑IV might have effects on endothelial function and ISNA. We performed in vitro experiments on endothelial cells. Being treated with different concentrations of magnesium or/and AS-IV, the cell growth and migration were detected by CCK-8 and wound healing assay, respectively. The pro-inflammatory factors tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), adhesion molecule vascular cell adhesion molecule-1 (VCAM-1), and NF-kB were determined by qRT-PCR, ELISA kits or western blot. Results showed that high magnesium and AS-IV improved endothelial function, including promoting cell migration and decreasing the content of TNF-α, IL-6, VCAM-1, and NF-kB. With the supplement of AS-IV, additive magnesium maintains cell proliferation, migration, and function of endothelial cells. In conclusion, these findings suggest that high magnesium and AS‑IV could improve vascular endothelial dysfunction. Early detection and treatment for neo-atherosclerosis may be of great clinical significance for improving stent implantation efficacy and long-term prognosis.

Background:Cerebral ischaemia-reperfusion injury (CIRI) could worsen the inflammatory response and oxidative stress in brain tissue. According to previous studies, ferulic acid methyl ester (FAME), as the extract with the strongest comprehensive activity in the traditional Chinese medicine Huang Hua oil dot herb, has significant anti-oxidative stress and neuroprotective functions, and can effectively alleviate CIRI, but its mechanism of action is still unclear. Methods:Firstly, the pharmacological effects of FAME were investigated by in vitro oxidative stress and inflammatory experiments. Secondly, evaluate the therapeutic effects of FAME in the treatment of CIRI by brain histopathological staining and cerebral infarct area by replicating the in vivo MACO model. Thirdly, RNA-Seq and network pharmacology were utilized to predict the possible targets and mechanisms of FAME for CIRI at the molecular level. Finally, the expression of key target proteins, as well as the key regulatory relationships were verified by molecular docking visualization, Western Blotting and immunohistochemistry. Results:The results of in vitro experiments concluded that FAME could significantly reduce the content of TNF-α, IL-1β and ROS, inhibiting COX-2 and iNOS protein expression in cells(p<0.01). FAME was demonstrated to have anti-oxidative stress and anti-inflammatory effects. The results of in vivo experiments showed that after the administration of FAME, the area of cerebral infarction in rats with CIRI was reduced, the content of Bcl-2 and VEGF was increased(p<0.05). Network pharmacology and RNA-Seq showed that the alleviation of CIRI by FAME may be through PI3K-AKT and HIF-1 signaling pathway. Enhanced expression of HIF-1α, VEGF, p-PI3K, p-AKT proteins in the brain tissues of rats in the FAME group was verified by molecular docking and Western Blotting. Conclusion:FAME possesses significant anti-inflammatory and anti-oxidative stress activities and alleviates CIRI through the PI3K/HIF-1α/VEGF signaling pathway.

Arisaema cum Bile (Dan Nanxing in Chinese, DNX) have been employed to treat allergic asthma. However, the active components and its mechanisms remain unknown. Therefore, the systematic pharmacology approach-experimental validation was performed in this study. Each 5, 6, and 10 compounds of DNX were obtained by HPLC analysis, TCMSP, and literature report, respectively. A total of 379 targets on all these compounds were acquired from Swiss Target Prediction, and 1973 targets on allergic asthma were predicated. The KEGG enrichment analysis was performed. Furthermore, a rat model of allergic asthma was established and DNX (450 mg/kg, p.o.) was given for 2 weeks. DNX treatment prevented OVA-induced pathological changes in lung cell of irregular arrange and necrotic bronchial epithelial. It also decreased inflammatory cytokines IL-4, IL-5, and IL-13 of serum and BALF, and increased IL-12 and IFN-γ. The main MAPK signaling pathway predicted by KEGG enrichment was verified, as indicated by the decreased protein expression of JNK (p < 0.05 & p < 0.01), ERK (p < 0.05), and p38 MAPK (p < 0.01) in lung tissue. These findings indicated that DNX attenuated OVA-induced allergic asthma mainly by decreasing the MAPK signaling pathway.

The effectiveness of herbal medicine in treating diabetes has grown in recent years, but the precise mechanism by which it does so is still unclear to both medical professionals and diabetics. In traditional Chinese medicine, mulberry leaf is used to treat inflammation, colds, and antiviral illnesses. Mulberry leaves are one of the herbs with many medicinal applications, and as mulberry leaf study grows, there is mounting evidence that these leaves also have potent anti-diabetic properties. The direct role of mulberry leaf as a natural remedy in the treatment of diabetes has been proven in several studies and clinical trials. However, because mulberry leaf is a more potent remedy for diabetes, a deeper understanding of how it works is required. The bioactive compounds flavonoids, alkaloids, polysaccharides, polyphenols, volatile oils, sterols, amino acids, and a variety of inorganic trace elements and vitamins, among others, have been found to be abundant in mulberry leaves. Among these compounds, flavonoids, alkaloids, polysaccharides, and polyphenols have a stronger link to diabetes. Of course, trace minerals and vitamins also contribute to blood sugar regulation. Inhibiting alpha glucosidase activity in the intestine, regulating lipid metabolism in the body, protecting pancreatic -cells, lowering insulin resistance, accelerating glucose uptake by target tissues, and improving oxidative stress levels in the body are some of the main therapeutic properties mentioned above. These mechanisms can effectively regulate blood glucose levels. The therapeutic effects of the bioactive compounds found in mulberry leaves on diabetes mellitus and their associated molecular mechanisms are the main topics of this paper’s overview of the state of the art in mulberry leaf research for the treatment of diabetes mellitus.

阿尔茨海默症(Alzheimer′s disease,AD)为一种致病机制尚不明确的神经退行性疾病,其中 β-淀粉样蛋白的积累、磷酸 tau 蛋白的神经原纤维缠结的形成以及有害的神经炎症是 AD 进展的主要标志性特征[1-3].全世界现约有 5000 万 AD 患者,预计到 2050 年将增加到 1.52 亿,AD 治疗药物有着巨大的临床规模需求[4].

Aim: Chaihu-jia-Longgu-Muli-tang (CLM) is derived from “Shang Han Lun” and is traditionally prescribed for treating depression. However, there is still a lack of evidence for its antidepressant effects, and the underlying mechanism is also unclear. This study aimed to assess clinical evidence on the efficacy of CLM in patients with depression using a meta-analysis and to explore its underlying antidepressant molecular mechanisms via network pharmacology.Methods: Eight open databases were searched for randomized controlled trials (RCTs) comparing the effects of CLM alone or combined with serotonin-norepinephrine reuptake inhibitors (SNRIs) and selective serotonin reuptake inhibitors (SSRIs) in patients with depression, evaluating the total effective rate of the treatment group (CLM alone or combined with SSRIs/SNRIs) and the control group (SNRIs or SSRIs), and comparing changes in depression scale, anxiety scale, sleep scale, inflammation indicators and adverse effects. Subsequently, the active ingredients and target genes of CLM were screened through six databases. Then Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and protein-protein interaction (PPI) network and topology analysis were performed. Finally, Molecular docking was applied to evaluate the binding affinity between components and predicted targets.Results: Twenty-four RCTs with a total of 2,382 patients were included. For the efficacy of antidepression and adverse effects, whether CLM alone or in combination with SSRIs/SNRIs, the treatment group has no inferior to that of the control group. Additionally, the intervention of CLM + SSRI significantly improved the symptoms of anxiety and insomnia, and reduced serum IL-6 and TNF-α levels. For network pharmacology, a total of 129 compounds and 416 intersection targets in CLM were retrieved. The interaction pathway between CLM and depression is mainly enriched in PI3K-Akt, JAK-STAT, and NF-κB signaling pathway, PIK3R1, MAPK3, and AKT1 may be the potential targets of Stigmasterol, β-stiosterol, coumestrol.Conclusion: Compared to SSRIs/SNRIs alone, CLM is more effective and safe in treating depression. It not only significantly alleviates depressive mood, but improves symptoms such as anxiety and insomnia, with fewer side effects, especially in combination with SSRI. Its antidepressant mechanism may be correlated with the regulation of the PI3K/Akt signaling pathway and inhibiting inflammatory response.

Oral bioavailability (F) is one of the key factors that need to be determined in drug discovery. This factor is determined by the permeability and solubility of new molecule entities (NMEs) according to the biopharmaceutics classification system (BCS). In the present study, we evaluated the permeability of 22 drugs in rat intestinal tissues using an Ussing chamber system and correlated the permeability with data on human intestinal absorption (Fa) and intestinal availability (Fa × Fg) reported in the literature. The rat intestinal permeability data were better correlated with the combined effect of the absorbed fraction (Fa) and the fraction escaping intestinal metabolism (Fg) than Fa itself. Clear regional dependent absorption was observed for most of the test drugs, and ileal Papp was generally higher than that in other segments. Finally, the function of the efflux transporter P-glycoprotein (P-gp) with regard to oral absorption of substrates was evaluated with an Ussing chamber. We also demonstrated that the rat intestinal stability of the three cytochrome P450 (CYP) substrates was consistent with the human data. An Ussing chamber system incorporating rat intestinal tissue would be a valuable tool to predict human intestinal absorption and metabolism for molecules with various physicochemical properties.

胃肠积热是无形或有形热邪壅于胃肠,致胃肠气分热盛的证候,病位涉及胃、大肠,多见于小儿,以手足心热、唇红、食欲异常、夜卧不安、大便干结、小便黄、舌质红苔黄厚、脉滑等为主要临床表现[1],饮食积滞是其形成的主要原因.小儿脏腑娇嫩,肺常不足,易受外邪侵袭,邪气入肺易化热,与壅于胃肠之热上下相搏发为肺胃(肠)积热证,可出现发热、咳嗽、扁桃体炎、鼻炎、肺炎喘嗽、便秘、遗尿、尿血、抽动障碍等症状.

目的 研究黄芩苷对多重耐药铜绿假单胞菌(MDRPA)慢性肺部感染大鼠的影响.方法 将32只SPF级雄性SD大鼠(6～8周龄,体重180～220g)采用随机数字表法分为空白组、模型组、西药组和黄芩苷组,每组8只.其中模型组、西药组和黄芩苷组采用经口气管插管法注入MDRPA藻酸盐包被体建立MDRPA慢性肺部感染大鼠模型.黄芩苷组给予0.8g/(kg·d)黄芩苷灌胃,西药组给予0.8g/(kg·d)哌拉西林他唑巴坦钠肌肉注射;空白组、模型组均给予与黄芩苷组等量的生理盐水灌胃.干预14 d后留取四组血清和肺组织,采用苏木精-伊红染色观察肺组织;酶联免疫吸附试验检测血清中肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)水平;实时定量聚合酶链反应检测肺组织Toll样受体4(TLR4)、核因子κB(p65亚基)(NF-κB p65)mRNA的表达.结果 空白组肺组织形态结构正常;模型组肺组织可见大量炎症细胞浸润,肺泡壁显著增厚;黄芩苷组肺组织浸润的炎症细胞较少,肺泡壁较薄.模型组血清TNF-α水平及肺组织TLR4、NF-κB p65 mRNA水平均高于空白组,血清IL-10水平低于空白组(P＜0.05).黄芩苷组血清TNF-α水平及肺组织TLR4、NF-κB NF-κB p65 mRNA水平均低于模型组,血清IL-10水平高于模型组(P＜0.05).结论 黄芩苷可以减轻MDRPA慢性肺部感染大鼠肺组织炎症损伤,其机制可能与抑制TLR4/NF-κB通路的激活相关.

手足口病(hand foot and mouth disease,HFMD)是由肠道病毒感染引起的一种儿童常见传染病,主要症状为手足肌肤、口咽部的疱疹.在过去15年内主要以环太平洋地区病例报告为主,我国HFMD的发病率、病死率位列全球首位[1].中西医在防治该病的过程中起着相辅相成的作用,现将其研究概况综述如下.

Ethnopharmacological relevance: In traditional Chinese Medicine, Rehmannia glutinosa (Gaertn.) DC., as the principle herb of ShengDiHuang Decotion (SDHD), has the effect of cooling blood and hemostasis, and tonifying the yin and kidney. Rheum L., as adjuvant herbs, assist Rehmannia glutinosa (Gaertn.) DC. to promote blood circulation to remove blood stasis. Aim of study: To study the mechanism of Rhein (RH) involved in the promotion of Rehmannioside D (RD) ab-sorption by pharmacokinetic studies, single-pass intestinal perfusion, Caco-2 cell models, molecular docking technique and western blotting. Materials and methods: Initially, the intestinal absorption of RD in the presence or absence of RH was conducted through pharmacokinetic studies. Thereafter, the intestinal absorption of RD and RH was studied using the single-pass intestinal perfusion and Caco-2 cell models. Finally, using molecular docking technique and western blotting. Results: We found that the promotion of RD absorption by RH was mediated by breast cancer resistance and multidrug resistance-associated protein 2, thereby affecting the permeability of the intestinal epithelium. Additionally, RH and RD can competitively bind to breast cancer resistance and multidrug resistance-associated protein 2, and that RH inhibits the expression of breast cancer resistance and multidrug resistance-associated protein 2 in the ileum to promote the intestinal absorption of RD. Conclusion: This study reveals the mechanisms associated with the RH-mediated promotion of RD absorption and provides a basis for further exploring the synergistic effect of Rehmannia glutinosa (Gaertn.) DC and rhubarb.