BACKGROUND:Obesity-induced adipose tissue expansion is characterized by capillary rarefaction and hypoxia, which disrupts angiogenesis and impairs beige adipogenesis. While angiogenesis is known to be crucial for beiging, the functional link between impaired vascularization and defective browning remains poorly understood. How natural compounds like berberine (BBR) links angiogenesis with beige adipogenesis remains unexplored. METHODS:Using both diet-induced obese (DIO) C57BL/6 J and leptin-deficient (ob/ob) murine models, we administered intraperitoneal BBR for 4 weeks. Adipose tissue remodeling was evaluated through histomorphometry, immunofluorescence, and flow cytometry. RNA sequencing of adipose tissue was performed to identify the potential targets. Chemical hypoxia was induced using CoCl₂ in preadipocytes to examine its effects on browning. RESULTS:BBR improved adipose tissue dysfunction in both the DIO model and the ob/ob model. It increased CD34+CD31+ endothelial progenitor cells and enhanced protein levels of VEGF/VEGFR2, PRDM16, PPAR-γ, and UCP-1, indicating simultaneous promotion of angiogenesis and adipose browning. Transcriptomic analysis revealed glutathione peroxidase 3 (GPx3) as a novel target through which BBR alleviates adipose dysfunction. GPX3 knockdown in vivo impaired angiogenesis and suppressed browning markers. BBR reversed chemical hypoxia-induced impairment of beige adipocyte differentiation independently of UCP-1 upregulation by inhibiting HIF-1α activation. CONCLUSIONS:This study unveils that BBR counteracts obesity-associated adipose tissue dysfunction: it upregulates GPx3 to reduce oxidative stress, which in turn normalizes HIF-1α levels and activates the PRDM16 signaling, thereby concurrently restoring adipose angiogenesis and promoting beige adipogenesis. This breaks the vicious cycle of hypoxia-impaired angiogenesis and suppressed thermogenesis, positioning BBR as a promising multi-target therapy for obesity.

BACKGROUND:Hyperuricemia and hypertension are prevalent chronic diseases that often co-occur. While numerous observational studies suggest an association between serum uric acid (SUA) levels and hypertension, the causal nature of this relationship remains unresolved due to confounding and reverse causation. This study systematically investigates the causal association between SUA levels and hypertension risk using Mendelian randomization (MR) methodologies. METHODS:We utilized single nucleotide polymorphisms (SNPs) identified in large-scale genome-wide association studies (GWAS) of European populations as genetic instruments for SUA levels. MR, a genetic epidemiology technique, uses genetic variations as proxies to mimic a randomized controlled trial and minimizing biases from confounding and reverse causation. Systolic and diastolic blood pressure (SBP and DBP) were the primary outcomes of interest. A two-sample MR analysis was conducted to assess the causal relationships, complemented by sensitivity analyses (weighted median, weighted mode, MR-Egger) to ensure result robustness. Findings are expressed as odds ratios (ORs) with 95% confidence intervals (Cis) per one standard deviation (SD) increase in SUA levels. RESULTS:Our MR analysis identified a significant causal effect of SUA levels on hypertension risk. Specifically, genetically predicted SUA levels were positively associated with SBP (β = 0.136 [0.035-0.238], p < .05) and DBP (β = 0.108 [0.007-0.209], p < .05).Conversely, reverse MR analysis revealed no significant causal effect of SBP (b = 0.058 [ - 9.52E-05-0.116],p = .0504] or DBP (β = 0.016 [ - 0.028-0.059], p > .05] on SUA levels, confirming the unidirectional nature of this association. CONCLUSION:This study provides compelling evidence from MR supporting a unidirectional causal link between SUA levels and increased hypertension risk. Unlike prior observational studies, our genetic approach effectively mitigates confounding and reverse causation, offering novel insights into the etiology of hypertension. These findings highlight the clinical importance of managing SUA levels to mitigate hypertension risk. Further research, including randomized controlled trials, is needed to confirm these findings and explore potential therapeutic interventions targeting SUA.

Background:Cynanchum paniculatum (Bunge) Kitag. ex H.Hara, a member of the Asclepiadaceae family, has a rich history as a traditional Chinese medicinal plant used to treat digestive disorders. However, its potential anti-cancer effects in pancreatic cancer remain largely unexplored.Aim: This study delves into the intricate anti-pancreatic cancer mechanisms of C. paniculatum (Bunge) Kitag. ex H.Hara aqueous extract (CPAE) by elucidating its role in apoptosis induction and the inhibition of invasion and migration.Methods: A comprehensive set of methodologies was employed to assess CPAE’s impact, including cell viability analyses using MTT and colony formation assays, flow cytometry for cell cycle distribution and apoptosis assessment, scratch-wound and Matrigel invasion assays for migration and invasion capabilities, and immunoblotting to measure the expression levels of key proteins involved in apoptosis and metastasis. Additionally, a murine xenograft model was established to investigate CPAE’s in vivo anti-cancer potential.Results: CPAE exhibited time- and dose-dependent suppression of proliferation and colony formation in pancreatic cancer cells. Notably, CPAE induced apoptosis and G2/M phase arrest, effectively activating the caspase-dependent PARP pathway. At non-cytotoxic doses, CPAE significantly curtailed the metastatic abilities of pancreatic cells, effectively suppressing epithelial-mesenchymal transition (EMT) and downregulating the TGF-β1/Smad2/3 pathway. In vivo experiments underscored CPAE’s ability to inhibit tumor proliferation.Conclusion: This study illuminates the multifaceted anti-proliferative, pro-apoptotic, anti-invasive, and anti-migratory effects of CPAE, both in vitro and in vivo. CPAE emerges as a promising herbal medicine for pancreatic cancer treatment, with its potential mediated through apoptosis induction via the caspase-dependent PARP pathway and MET suppression via the TGF-β1/Smad2/3 signaling pathway at non-cytotoxic doses. These findings advocate for further exploration of CPAE’s therapeutic potential in pancreatic cancer.

Adipose tissue senescence is a precursor to organismal aging and understanding adipose remodelling contributes to discovering novel anti-aging targets. Glutathione peroxidase 3 (GPx3), a critical endogenous antioxidant enzyme, is diminished in the subcutaneous adipose tissue (sWAT) with white adipose expansion. Based on the active role of the antioxidant system in counteracting aging, we investigated the involvement of GPx3 in adipose senescence. We determined that knockdown of GPx3 in adipose tissue by adeno-associated viruses impaired mitochondrial function in mice, increased susceptibility to obesity, and exacerbated adipose tissue senescence. Impairment of GPx3 may cause mitochondrial dysfunction through inner mitochondrial membrane disruption. Adipose reshaping management (cold stimulation and intermittent diet) counteracted the aging of tissues, with an increase in GPx3 expression. Overall metabolic improvement induced by cold stimulation was partially attenuated when GPx3 was depleted. GPx3 may be involved in adipose browning by interacting with UCP1, and GPx3 may be a limiting factor for intracellular reactive oxygen species (ROS) accumulation during stem cell browning. Collectively, these findings emphasise the importance of restoring the imbalanced redox state in adipose tissue to counteract aging and that GPx3 may be a potential target for maintaining mitochondrial homeostasis and longevity.

Objective To evaluate the efficacy of Huachansu tablets combined with transarterial chemoembolization (TACE) for treatment of primary hepatocellular carcinoma (HCC) and prognostic influence factors. Methods One hundred and eight patients with HCC were recruited according to the inclusion and exclusion criteria. Patients were randomly divided into treatment group and control group. The treatment group was treated with Huachansu tablets combined with TACE, and the control group was treated with TACE alone, with overall survival time (OS) and progression-free survival time (PFS) as the evaluation indexes. The COX regression analysis was used to evaluate the survival and prognostic effects and their influence factors in both groups. Results A total of 108 HCC patients were enrolled. The OS was 13.5 months in treatment group and 9.2 months in control group; the PFS was 6.8 months in treatment group and 5.3 months in control group, and the differences were significant statistically (all P<0.05). Multivariate COX regression analysis showed that Child-Pugh grade and cirrhosis were the independent risk factors for PFS in HCC patients. Child-Pugh grade were the independent risk factors for OS in HCC patients. ALBI is a protective factor for OS in HCC patients. Conclusions The treatment of HCC by Huachansu tablets combined with TACE can delay the progression of HCC and prolong PFS and OS of the patients with HCC. Child-Pugh grade, cirrhosis status, and ALBI were important factors affecting the prognosis of the patients with HCC.

目的 观察血府逐瘀汤对血瘀证的结直肠癌伴抑郁、焦虑患者的临床疗效及肠道代谢产物的影响.方法 将2019年1月～ 2022年1月上海交通大学医学院附属瑞金医院收治的120例血瘀证型Ⅲ期结直肠癌伴抑郁、焦虑患者,随机分为治疗组和对照组,每组60例.治疗组给予血府逐瘀汤口服,对照组给予安慰剂口服.3个月后比较分析两组心理量表(包括SDS、SAS、HAMD、HAMA)、中医症状评分、无疾病生存期(disease free survival,DFS)及代谢组学.结果 治疗后,组内比较,治疗组的乏力得分较前增加(P＜0.05),量表(SDS、SAS、HAMD、HAMA)、不寐、脘腹胀满、心烦易怒得分较前明显下降(P＜0.01);对照组HAMD、HAMA、不寐、乏力得分较前明显下降(P＜0.01).两组间比较,治疗组SDS、HAMD、不寐、心烦易怒得分均低于对照组(P＜0.05),HAMA、脘腹胀满得分明显低于对照组(P＜0.01).治疗组DFS为38.72±2.22个月,较对照组延长2个月(P＞0.05).两组肠道代谢产物差异分析主要为脯氨酸、6-羟基烟酸、丝氨酸、肌醇、丙二酸、阿魏酸、吲哚丁酸、丁酸等.结论 中药血府逐瘀汤可改善结直肠癌的抑郁、焦虑,调节肠道代谢,延长无疾病生存期.

目的:探讨新型小分子抗病毒药物临床使用的药学监护模式.方法:临床药师对 2例肺部感染患者使用不同的小分子抗病毒药物后发生不良反应的治疗过程进行分析总结.探讨小分子抗病毒药物引发不良反应发生的影响因素,协助医师评价可疑药物和处理不良反应.结果:通过与临床医生协同处理不良反应,患者不良反应情况明显改善后出院.结论:临床药师通过参与药学监护,体现了临床药师的服务价值,保障了临床用药的有效性安全性.

BACKGROUND:Breast cancer is one of the most common cancers in women, affecting more than 2 million women worldwide annually. However, effective treatments for breast cancer are limited. Nobiletin is a flavonoid present in the dried mature pericarp of mandarin orange (Citrus reticulata Blanco), which is used to prepare Citri Renetulatae Pericarpium and can inhibit tumour growth and progression according to modern pharmacological studies. However, whether nobiletin exhibits an antimetastatic role in breast cancer and its potential mechanism need to be further investigated.PURPOSE:This study aims to evaluate the inhibitory effect of nobiletin on breast cancer and to elucidate potential mechanisms against invasion and migration.METHODS:Cell viability was determined by cell counting kit-8 and colony formation assays. Wound healing and Boyden chamber assays detected cancer cell migration and invasion capabilities. Immunoblotting and qPCR were applied to determine the protein and mRNA expression levels of extracellular signal-regulated kinases (ERK) and the c-Jun N-terminal kinase (JNK) signalling pathways. Molecular docking was used to assess the degree of nobiletin binding to phosphatidylinositol 3-kinase (PI3K). Xenografts and liver metastases were constructed in BALB/c nude mice to evaluate the anticancer effect of nobiletin in vivo. H&E staining and immunohistochemistry were used to detect proliferation and the expression of related proteins.RESULTS:Nobiletin induced cell death in a concentration- and time-dependent manner and possessed anti-invasion and anti-migration effects on MCF-7 and T47D cells by suppressing the interleukin-6-induced ERK and JNK signalling pathways. In addition, nobiletin docked with the binding site of PI3K, and the binding score was -8.0 kcal/mol. Furthermore, the inhibition of breast cancer growth and metastasis by nobiletin was demonstrated by constructing xenografts and liver metastases in vivo.CONCLUSION:Nobiletin inhibited liver metastasis of breast cancer by downregulating the ERK-STAT and JNK-c-JUN pathways, and its safety and efficacy were verified, indicating the potential of nobiletin as an anticancer agent.

目的:观察扶中消积法(FZXJF)治疗结直肠癌的临床疗效及对生存状况的影响.方法:研究设计基于真实世界理论,收集符合纳入标准的结直肠癌患者,根据患者是否服中药的意愿分为对照组和观察组.对照组采用西医标准放化疗等治疗,观察组在西医治疗的基础上,同时给予FZXJF组方中药口服,每日1剂.观察两组患者的总生存期、无进展生存期、症状缓解时间.同时根据生存状态的影响因素,建立结直肠癌预测模型.结果:结直肠癌患者中,观察组总生存期(OS)为(89.08±2.67)月,对照组OS为(73.33±4.05)月,差异有统计学意义(P＜0.01)其中:①Ⅱ期患者中,观察组OS为(113.37±2.10)月,对照组OS为(96.58±4.11)月,差异无统计学意义(P＞0.05);②Ⅲ期患者中,观察组OS为(96.26±2.75)月,对照组OS为(89.44±6.69)月,差异无统计学意义(P＞0.05);③Ⅳ期患者中,观察组OS为(52.92±3.93)月,对照组为(41.23±4.35)月,差异有统计学意义(P＜0.05).Cox回归分析表明,口服中药可以降低死亡风险57.63％,差异有显著统计学意义(P＜0.01);肿瘤分期较高是肿瘤患者生存状态的危险因素,尤其是Ⅳ期患者,差异有统计学意义(P＜0.05).Cox回归因素分析基础上,加入中医药治疗后,计算调整后的模型曲线下面积(AUC)为0.71,预测的区分度属于中等.结论:FZXJF可延长结直肠癌Ⅱ、Ⅲ、Ⅳ患者的生存期,对Ⅳ期患者尤为显著(P＜0.05).中药可改善结直肠癌患者的预后,延长生存期.

Objective: Erchen Decoction (ECD), a well-known traditional Chinese medicine, exerts metabolism-regulatory, immunoregulation, and anti-tumor effects. However, the action and pharmacological mechanism of ECD remain largely unclear. In the present study, we explored the effects and mechanisms of ECD in the treatment of CRC using network pharmacology, molecular docking, and systematic experimental validation. Methods: The active components of ECD were obtained from the TCMSP database and the potential targets of them were annotated by the STRING database. The CRC-related targets were identified from different databases (OMIM, DisGeNet, GeneCards, and DrugBank). The interactive targets of ECD and CRC were screened and the protein-protein interaction (PPI) networks were constructed. Then, the hub interactive targets were calculated and visualized from the PPI network using the Cytoscape software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. In addition, the molecular docking was performed. Finally, systematic in vitro, in vivo and molecular biology experiments were performed to further explore the anti-tumor effects and underlying mechanisms of ECD in CRC. Results: A total of 116 active components and 246 targets of ECD were predicted based on the component-target network analysis. 2406 CRC-related targets were obtained from different databases and 140 intersective targets were identified between ECD and CRC. 12 hub molecules (STAT3, JUN, MAPK3, TP53, MAPK1, RELA, FOS, ESR1, IL6, MAPK14, MYC, and CDKN1A) were finally screened from PPI network. GO and KEGG pathway enrichment analyses demonstrated that the biological discrepancy was mainly focused on the tumorigenesis-, immune-, and mechanism-related pathways. Based on the experimental validation, ECD could suppress the proliferation of CRC cells by inhibiting cell cycle and promoting cell apoptosis. In addition, ECD could inhibit tumor growth in mice. Finally, the results of molecular biology experiments suggested ECD could regulate the transcriptional levels of several hub molecules during the development of CRC, including MAPKs, PPARs, TP53, and STATs. Conclusion: This study revealed the potential pharmacodynamic material basis and underlying molecular mechanisms of ECD in the treatment of CRC, providing a novel insight for us to find more effective anti-CRC drugs.

血管内皮生长因子抑制剂(VEGFR)广泛用于恶性肿瘤晚期治疗.高血压、血栓事件、心脏毒性是VEGFR最为常见的心血管不良事件.研究显示,降低体内NO和前列腺素的释放;损伤血管内皮,激活凝血因子;"靶向"与"脱靶"作用是引起此类心血管事件的主要机制.中医药除了有抗肿瘤的作用外,也能减轻肿瘤治疗中的心血管不良事件.该文就抗血管生成靶向药物的主要心血管事件机制及相应的中医药治疗进行整理.

Objective. This study aimed to evaluate the effectiveness and safety of Fuzheng Xiaoji granule in patients with stage IIIC colorectal cancer. Methods. A total of 150 patients with stage IIIC colorectal cancer treated in Shanghai Ruijin Hospital from January 2019 to January 2022 were selected. They were divided into treatment and control groups according to a 2 : 1 random number table. There were 100 cases in the treatment group and 50 cases in the control group. The treatment group was administered Fuzheng Xiaoji (FZXJ) granule, and the control group was administered the placebo orally. The primary endpoint was disease-free survival (DFS). In addition, after 6 months, the changes in Traditional Chinese Medicine (TCM) symptom score (fatigue, emotional depression, chest tightness, insomnia, anorexia, abdominal distension, abdominal pain, soreness and weakness in the waist and legs, chills, and dysphoria in the chest, palm, and soles) were compared. Results. The DFS was 34.37 ± 2.91 months in the control group and 37.0 ± 1.08 months in the treatment group ( p < 0.05 ). Compared with the control group, the treatment group showed less fatigue, abdominal distension, and soreness and weakness in the waist and legs ( p < 0.05 ), significantly. The scores of emotional depression and anorexia decreased obviously, with a significant difference between the control and treatment groups ( p < 0.01 ). There were no significant differences between the control and treatment groups in the incidence of chest tightness, insomnia, abdominal pain, chills, and dysphoria in the chest, palm, and soles ( p > 0.05 ). Conclusion. Fuzheng Xiaoji granule can improve patients’ symptoms and prolong the DFS.

Ethnopharmacological relevance: Fuzheng Xiaojijinzhan (FZXJJZF) decoction is an effective prescription for treating colorectal cancer liver metastasis (LMCRC). Aim of the study: To elucidate the pharmacological mechanism of the FZXJJZF decoction therapy on LMCRC. Materials and methods: Firstly, a network pharmacological approach was used to characterize the underlying targets of FZXJJZF on LMCRC. Secondly, LMCRC-related genes are obtained from the public database TCGA, and those genes are further screened and clustered through Mfuzz, an R package tool. Then, targets of FZXJJZF predicted by network pharmacology were overlapped with LMCRC related genes screened by Mfuzz. Meanwhile, FZJZXJF intervened in LMCRC model,epithelial-to-mesenchymal transition (EMT), and migration and invasion of HCT-116 cells. Thirdly, the transcriptomics data of FZJZXJF inhibited HCT-116 cells of EMT cells were overlapped with EMT database data to narrow the possible range of targets. Based on this, the potential targets and signal pathways of FZJZXJF were speculated by combining the transcriptomics data with the targets from network pharmacology-TCGA. Finally, the anti-cancer mechanism of FZXJJZF on LMCRC was verified in vitro by Real-Time PCR and Western Blot in vitro. Results: By network pharmacological analysis, 282 ingredients and 429 potential targets of FZXJJZF were predicted. The 9268 LMCRC-related genes in the TCGA database were classified into 10 clusters by the Mfuzz. The two clustering genes with the most similar clustering trends were overlapped with 429 potential targets, and 32 genes were found, such as CD34, TRPV3, PGR, VDR, etc. In vivo experiments, FZJZXJF inhibited the tumor size in LMCRC models, and the EMT, migration, and invasion of HCT-116 also be inhibited. Intersecting transcriptomics dates with 32 target genes, it is speculated that the VDR-TGF-beta signaling pathway may be an effective mechanism of FZXJJZF. Additionally, it is shown that FZXJJZF up-regulated the expression levels of VDR and E-cadherin and down-regulated the expression levels of TGF-beta and Snail1 in vitro. These results confirmed that FZXJJZF plays an effective role in LMCRC mainly by inhibiting EMT phenotype via the VDR-TGF-beta signaling pathway. Conclusions: Collectively, this study reveals the anti-LMCRC effect of FZXJJZF and its potential therapeutic mechanism from the perspective of potential targets and potential pathways.

Activation of inflammasomes has been reported in human pancreatic adenocarcinoma (PAAD); however, the expression pattern and functional role of inflammasome-related proteins in PAAD have yet to be identified. In this study, we systemically examined the expression and role of different inflammasome proteins by retrieving human expression data. Several genes were found to be differentially expressed; however, only interferon-inducible protein 16 (IFI16) expression was found to be adversely correlated with the overall survival of PAAD patients. Overexpression of IFI16 significantly promoted tumor growth, increased tumor size and weight in the experimental PAAD model of mice, and specifically increased the population of tumor-associated macrophages (TAMs) in the tumor microenvironment. Depletion of TAMs by injection of liposome clodronate attenuated the IFI16 overexpression-induced tumor growth in PAAD. In vitro treatment of conditioned medium from IFI16-overexpressing PAAD cells induced maturation, proliferation, and migration of bone marrow-derived monocytes, suggesting that IFI16 overexpression resulted in cytokine secretion that favored the TAM population. Further analysis suggested that IFI16 overexpression activated inflammasomes, thereby increasing the release of IL-1β. Neutralization of IL-1β attenuated TAM maturation, proliferation, and migration induced by the conditioned medium from IFI16-overexpressing PAAD cells. Additionally, knockdown of IFI16 could significantly potentiate gemcitabine treatment in PAAD, which may be associated with the reduced infiltration of TAMs in the tumor microenvironment. The findings of our study shed light on the role of IFI16 as a potential therapeutic target for PAAD.

目的:探讨莪术二酮对三阴性乳腺癌细胞MDA-MB-231增殖、凋亡和细胞周期的作用.方法:体外培养MDA-MB-231细胞,以卡培他滨作为阳性对照,采用细胞增殖与活性检测(CCK-8)法检测不同浓度的莪术二酮(125,250,500,1000,2000μmol· L-1)作用细胞24,48 h后对细胞活力的影响;选取3个有效抑制增殖的莪术二酮浓度(250,500,1000 μmol·L-1)进行后续实验.流式细胞术结合碘化丙啶(PI)染色法检测莪术二酮对细胞周期的影响;增设高浓度组(2000 μmol·L-1),用JC-1法检测莪术二酮对细胞线粒体膜电位的影响,并采用流式细胞术结合Annexin V-FITC/PI双染色法检测细胞凋亡的情况;蛋白免疫印迹法(Western blot)检测莪术二酮作用后细胞中周期调控和凋亡相关蛋白表达的变化.结果:与空白组比较,250,500,1000,2000 μmol·L-1莪术二酮对细胞增殖有显著抑制作用(P＜0.01),效果呈浓度和时间依赖性,24 h和48 h的半抑制浓度(IC50)分别为1607,1401μmol·L-1;250,500,1000 μmol·L-1莪术二酮可将细胞阻滞在G1期;250 μmo1·L-1莪术二酮对细胞线粒体膜电位无影响,500,1000,2000 μmo1·L-1莪术二酮可使细胞线粒体膜电位明显下降(P＜0.05,P＜0.01);250,500,1000 μmol·L-1莪术二酮可使凋亡细胞比例明显增加(P＜0.05,P＜0.01);各浓度莪术二酮可使B淋巴细胞瘤-2相关X蛋白(Bax)/B淋巴细胞瘤-2(Bcl-2)明显增加(P＜0.05,P＜0.01),半胱氨酸天冬氨酸蛋白水解酶-3(Caspase-3)蛋白表达量无明显变化,而Caspase-9,cleaved Caspase-9,cleaved Caspase-3,p53和p21蛋白表达量均有所增加(P＜0.05).结论:一定浓度的莪术二酮能抑制MDA-MB-231细胞的增殖,可能与其阻滞细胞周期、诱导细胞凋亡有关.

目的 观察表柔比星+奥沙利铂+5-氟尿嘧啶化疗方案联合生物治疗用于胃癌新辅助化疗的癌细胞杀伤效果.方法 选取在上海交通大学医学院附属瑞金医院接受术前新辅助化疗的胃癌患者100例,随机接受表柔比星+奥沙利铂+5-氟尿嘧啶化疗方案联合树突状细胞-细胞因子诱导的杀伤细胞(联合组)或表柔比星+奥沙利铂+5-氟尿嘧啶化疗方案(对照组),每组各50例,化疗前后测定血清肿瘤标志物的含量,化疗后测定手术切除病灶中增殖基因、抑癌基因的表达量并评估化疗有效率.结果 化疗后,对照组及联合组患者血清中CA72-4、G17、TK-1的含量均低于化疗前[联合组:CA72-4(27.11±3.85)ng/mL vs(55.27±7.68)ng/mL,G17(46.13±8.79)ng/mL vs(78.84±9.65)ng/mL,TK-1(1.32±0.31)pmol/mL vs(3.18±0.47)pmol/mL;对照组:CA72-4(39.83±5.12)ng/mL vs(54.76±8.14)ng/mL,G17(56.71±8.76)ng/mL vs(78.65±9.48)ng/mL,TK-1(2.26±0.33)pmol/mL vs(3.38±0.42)pmol/mL],且联合组低于对照组[CA72-4(27.11±3.85)ng/mL vs(39.83±5.12)ng/mL,G17(46.13±8.79)ng/mL vs(56.71±8.76)ng/mL,TK-1(1.32±0.31)pmol/mL vs(2.26±0.33)pmol/mL],差异有统计学意义(P<0.05);联合组患者手术切除病灶中各增殖基因mRNA表达量低于对照组[Cy-clinB:(0.32±0.04)vs(0.96±0.12),CyclinD1:(0.28±0.04)vs(1.02±0.11),CDK1:(0.41±0.04)vs(1.06±0.13),CDK4(0.77±0.03)vs(1.02±0.18),CDK6(0.24±0.06)vs(0.98±0.12)],差异有统计学意义(P<0.05);联合组患者手术切除病灶中各抑癌基因mRNA表达量低于对照组[RASSF1A(0.36±0.08)vs(1.00±0.09),Noxa(0.44±0.09)vs(1.02±0.18),CKN1(0.28±0.10)vs(1.03±0.15),p16ink4a(0.62±0.09)vs(0.99±0.12)],差异有统计学意义(P<0.05);联合组手术切除率以及根治性切除率均高于对照组(根治性切除率52.00％vs 30.00％,手术切除率70.00％vs 42.00％),差异有统计学意义(P<0.05);联合组不良反应发生率与对照组相比差异无统计学意义(30.00％vs 32.00％)(P>0.05);联合组有效率高于对照组(60.00％vs 40.00％),差异有统计学意义(P<0.05).结论 联合表柔比星+奥沙利铂+5-氟尿嘧啶化疗方案更为有效地杀伤胃癌细胞并抑制癌细胞增殖、侵袭,值得临床广泛推广和应用.

Citrus folium and its main ingredient nobiletin (NOB) have received widespread attention in recent years due to their antitumor effects. The antitumor effect of Citrus folium is related to the traditional use, mainly in its Chinese medicinal properties of soothing the liver and promoting qi, resolving phlegm, and dispelling stagnation. Some studies have proved that Citrus folium and NOB are more effective for triple-negative breast cancer (TNBC), which is related to the syndrome of stagnation of liver qi. From the perspective of modern biomedical research, NOB has anticancer effects. Its potential molecular mechanisms include inhibition of the cell cycle, induction of apoptosis, and inhibition of angiogenesis, invasion, and migration. Citrus folium and NOB can also reduce the side effects of chemotherapy drugs and reverse multidrug resistance (MDR). However, more research studies are needed to clarify the underlying mechanisms. The modern evidence of Citrus folium and NOB in breast cancer treatment has a strong connection with the traditional concepts and laws of applying Citrus folium in Chinese medicine (CM). As a low-toxic anticancer drug candidate, NOB and its structural changes, Citrus folium, and compound prescriptions will attract scientists to use advanced technologies such as genomics, proteomics, and metabolomics to study its potential anticancer effects and mechanisms. On the contrary, there are relatively few studies on the anticancer effects of Citrus folium and NOB in vivo. The clinical application of Citrus folium and NOB as new cancer treatment drugs requires in vivo verification and further anticancer mechanism research. This review aims to provide reference for the treatment of breast cancer by Chinese medicine.

This study aimed to explore the potential molecular mechanisms of FuZheng XiaoJi prescription (FZXJP) on Colorectal Cancer (CRC) cells. Transcriptome sequencing was performed on HT-29 cells treated with FZXJP and not followed by selecting differentially expressed genes (DEGs). Functional enrichment analysis and protein-protein interaction (PPI) analysis were performed for the DEGs. The transcription factors were predicted using TRRUST and miRWalk 3.0. Finally, Real-time PCR (qRT-PCR) was used to verify the results of transcriptome sequencing. HT-29 had a more sensitive response to FZXJP. Transcriptome sequencing revealed 1522 DEGs, and they were enriched in various biological processes and pathways, such as regulation of cellular biosynthetic process and MAPK signaling pathway. Totally 61 proteins in the PPI network with degree > 5 were screened as hub genes, including EGR1, KLHL11, UBA7, IRF1, HERC6, and IFI35. The qRT-PCR confirmed that the expression of those genes was consistent with that of transcriptome analysis. Three transcription factors and 15 miRNAs were predicted. All the three transcription factors were found to interact with EGR1. IRF1 was a target of miR-93-5p. This study provided a theoretical basis for the regulation of FZXJP in HT-29cells, which lays a foundation for the treatment of CRC.

时值金秋,气候宜人,可恼人的秋燥也如期而至.地铁上、车厢里、餐桌前,不时传来“咳咳咳”的声音.秋天的咳嗽困扰着很多人,空调族、老年人以及一部分儿童尤甚.俗话说,“秋养脏,肺至重”.那么,秋天燥咳怎么办? “燥咳”有哪些症状 秋季气候适宜病毒、细菌生长,一旦咳喘形成,同时伴有感染、自身体质易过敏等多重因素,就会出现鼻腔、口唇干燥,咽喉干痛,喜饮,并伴有咳嗽等表现.这种咳嗽与一般咳嗽的不同之处在于,其干咳无痰,或痰少而黏,不易咳出,或痰中带血丝,咽干,鼻唇干燥.这就是令人烦恼的秋燥咳嗽,中医称之为“燥咳”.

目的 观察中医经验方葛芪方辅助治疗2型糖尿病(T2DM)的临床疗效.方法 将80例T2DM患者随机分为治疗组和对照组,每组40例.两组患者均给予盐酸二甲双胍片治疗,治疗组加用中药葛芪方治疗,两组疗程均为3个月.比较两组患者治疗前后空腹血糖、餐后2h血糖(2hPBG)、糖化血红蛋白(HbA1c)、体质指数、血脂、C反应蛋白(CRP)水平及稳态模型评价胰岛素抵抗(HOMA-IR)指数的变化.结果 治疗后,治疗组患者空腹血糖、2hPBG、HbA1c、HOMA-IR指数均低于对照组(均P＜0.05),两组血脂、体质指数、CRP水平均无统计学差异(均P＞0.05).结论 葛芪方辅助治疗T2DM能更有效地降低患者血糖,减轻胰岛素抵抗.