Background: As a common clinical anticancer drug, doxorubicin (DOX) easily triggers obvious doxorubicin-induced cardiotoxicity (DIC) during clinical application. Accumulating evidence has proven that ferroptosis dominates the pathological process of DIC yet efficient targeted treatment strategies remain scarce. The present work mainly focused on clarifying the protective role of quercetin (QUE) against DIC. Methods: In vivo rat models and in vitro cardiomyocyte injury models were constructed to mimic DIC. Echocardiographic detection and histological staining were adopted to observe overall cardiac function and myocardial fibrotic changes. Ultrastructural alterations of intracellular mitochondria were observed under a transmission electron microscope. Relevant ferroptosis and oxidative stress levels were further determined. Moreover, a Western blot assay and NRF2 gene transfection technique were applied to confirm the involvement of the NRF2 signaling pathway. Results: In vivo and in vitro experimental outcomes showed that QUE treatment effectively relieved abnormal cardiac function and myocardial fibrotic lesions and improved damaged mitochondrial morphology. It also markedly restrained excessive iron accumulation and abnormal lipid peroxidation and restored disturbed redox balance in cardiomyocytes. Further mechanism exploration revealed that QUE could facilitate NRF2 entry into the cell nucleus and activate downstream SLC7A11/GPX4 signaling to maintain cellular glutathione homeostasis. Silencing NRF2 expression could fully reverse the above beneficial influences of QUE. Conclusions: Collectively, our experimental data demonstrated that QUE confers cardioprotective effects against DIC within subacute rat models and cultured cardiomyocyte injury models. Further mechanistic observations revealed that this protective phenotype is closely linked to the activation of NRF2/SLC7A11/GPX4 signaling alongside obvious reductions in multiple characteristic ferroptosis markers.

Doxorubicin (DOX) is a potent chemotherapeutic agent widely used in the clinical treatment of various malignancies. However, its therapeutic application is significantly constrained by dose-dependent cardiotoxicity, with accelerated cardiac aging emerging as a particularly challenging issue. This presents a critical limitation to its clinical use, emphasizing the urgent need for targeted cardioprotective strategies to mitigate DOX-induced cardiotoxicity. Cellular senescence, marked by permanent cell cycle arrest, plays a key role in the development of DOX-induced cardiac aging. DOX has been shown to induce cellular stress and senescence in multiple cardiac cell types, leading to impaired cardiac function. Understanding the molecular pathways and mechanisms through which DOX triggers cardiac aging is essential for the development of effective interventions to address its cardiotoxic side effects. In this review, we discuss the molecular mechanisms underlying DOX-induced senescence in different cardiac cell types and summarize the current progress in anti-aging therapeutic strategies aimed at alleviating DOX-related cardiac complications.

Doxorubicin (DOX) is a widely used anthracycline chemotherapeutic agent; however, its clinical application is limited by dose-dependent cardiotoxicity, which can result in progressive cardiac dysfunction and heart failure. Increasing evidence indicates that DOX-induced cardiotoxicity is closely associated with premature cardiac senescence, a pathological process distinct from physiological cardiac aging. DOX induces senescence-associated alterations in multiple cardiac cell populations, disrupting cardiac homeostasis and contributing to pathological remodeling. In this review, we summarize current advances in DOX-induced cardiac senescence, focusing on the contributions of different cardiac cell types, the underlying molecular mechanisms, and emerging therapeutic strategies. We further discuss the challenges and future perspectives for developing effective interventions that alleviate cardiac senescence while preserving the anticancer efficacy of DOX. Understanding the mechanisms driving DOX-induced cardiac senescence may provide new opportunities to develop effective cardioprotective strategies and improve long-term cardiac outcomes after chemotherapy.

Background Doxorubicin (DOX), a widely used chemotherapeutic agent, is limited in clinical application due to its dose-dependent cardiotoxicity. Therefore, it is crucial to explore alternative therapeutic molecules or drugs for mitigating DOX-induced cardiomyopathy (DIC). In this study aimed to explore underlying mechanisms of the cardioprotective effects of Kaempferol (KP) against DIC.Methods H9c2 cell-based DIC model were established to explore the pharmacological mechanism. The levels of mitochondrial membrane potential, mitochondrial ROS, mitochondrial Fe2+ and lipid peroxidation were detected using JC-1, TMRE, Mito-SOX, Mito-Ferro Green and C11-BODIPY 581/591 probes. Furthermore, Western blot analysis measured the expression of key regulatory proteins, and NRF2-targeting siRNA was transfected into H9c2 cells. The nuclear translocation of NRF2 was assessed by immunofluorescence.Results Data revealed that KP mitigated DOX-induced mitochondrial damage and ferroptosis via reducing membrane potential, mitochondrial ROS/Fe²+, and regulating lipid metabolism. Mechanistically, Western blot analysis revealed that KP inhibited DOX-induced ferroptosis by activating NRF2/SLC7A11/GPX4 axis. Moreover, KP promoted the accumulation and nuclear translocation of NRF2 protein.Conclusion These findings demonstrated that KP protected against DOX-induced myocardial damage by inhibiting mitochondrial ROS-dependent ferroptosis. This provides novel insights into KP as a promising drug candidate for cardioprotection.

Objective: This study aimed to investigate the formulation of Qing Xuan Decoction (QXD) and its possible mechanism of action in the treatment of opioid-induced constipation (OIC). Methods: We used orthogonal design experiments to optimize the decoction and ethanol precipitation process for QXD. The efficacy of QXD on loperamide - induced constipation in mice was explored via intestinal motility assay and defecation study. We examined the influence of QXD on the intestinal microbiota of mice through 16S rRNA sequencing. We assessed the alterations in the H2O2 and superoxide anion scavenging rates in serum using commercial kits. Results: The optimal decoction protocol for QXD entails boiling it with a 10 - fold volume of water for three consecutive cycles, each lasting 1.5 h. The optimized ethanol precipitation process requires using 85 % ethanol and performing the procedure three times, with each instance of precipitation lasting over 48 h. QXD enhanced small intestine propulsion rate and defecation efficacy, significantly ameliorating loperamide-induced constipation. QXD increased the abundance of Bacteroides, Prevotella, and Akkermansia in the intestine, decreased the abundance of Desulfovibrio, and kept the intestinal flora balanced. QXD mitigated oxidative stress by decreasing H₂O₂ levels and augmenting superoxide anion scavenging ability. Conclusion: QXD is expected to be a promising therapeutic drug for OIC, and its mechanism of action may be to alleviate constipation by regulating the homeostasis of intestinal flora while reducing oxidative stress.

Methyl mercaptan (CH3SH) is a malodorous and toxic gas commonly emitted from petrochemical, pharmaceutical, and wastewater treatment industries. Due to its low odor threshold and contribution to secondary atmospheric pollution, its effective removal is essential. Traditional methods, such as adsorption, absorption, biodegradation, and non-thermal plasma, often suffer from limitations in efficiency and stability. Catalytic technologies have garnered increasing attention for their high removal efficiency, low energy consumption, and environmental compatibility. This review highlights recent advances in the gas-phase catalytic elimination of CH3SH, focusing on reaction mechanisms, catalyst design, and performance metrics. Special emphasis is placed on strategies such as oxygen vacancy engineering, modulation of metal oxidation states, and interface/defect tuning to enhance catalytic activity and durability. Key performance factors are discussed, and current challenges are critically evaluated. Finally, future research directions are proposed to support the development of efficient and sustainable CH3SH abatement technologies.

Alzheimer's disease (AD)-related brain deterioration is linked to the type 2 diabetes mellitus (T2DM) features hyperglycemia, hyperinsulinemia, and insulin resistance. Hypoxia as a common risk factor for both AD and T2DM. Hypoxia-inducible factor-1 alpha (HIF-1α) acts as the main regulator of the hypoxia response and may be a key target in the comorbidity of AD and T2DM. HIF-1α expression is closely related to hyperglycemia, insulin resistance, and inflammation. Tissue oxygen consumption disrupts HIF-1α homeostasis, leading to increased reactive oxygen species levels and the inhibition of insulin receptor pathway activity, causing neuroinflammation, insulin resistance, abnormal Aβ deposition, and tau hyperphosphorylation. HIF-1α activation also leads to the deposition of Aβ by promoting the abnormal shearing of amyloid precursor protein and inhibiting the degradation of Aβ, and it promotes tau hyperphosphorylation by activating oxidative stress and the activation of astrocytes, which further exasperates AD. Therefore, we believe that HIF-α has great potential as a target for the treatment of AD. Importantly, the intracellular homeostasis of HIF-1α is a more crucial factor than its expression level.

Background: Alzheimer's disease (AD) is a neurological disorder. There is a considerable unmet medical need among those suffering from it. Hypothesis and purpose: Given the link between type-2 diabetes mellitus (T2DM) and AD, hypoglycemic traditional Chinese medicine formulas (TCMFs) may be a treatment for AD. We investigated the possibility of identifying anti-AD medicines in hypoglycemic TCMFs and presented another option for the screening of AD medications. Study design and methods: Paralysis of the transgenic Caenorhabditis elegans (C. elegans) strain CL4176 (caused by amyloid beta (AO)1-42 aggregates) was used to evaluate the anti-AD effect. The toxicity and neurodegeneration induced by neuronal expression of AO in the transgenic C. elegans strain CL2355 were determined using a 5-hydroxytryptamine (5-HT) assay. The transgenic AO-expressing strain CL 2006 and transgenic tau-expressing strain BR5270 were used to explore the effect of TCMFs on protein expression in C. elegans using ELISAs. Then, network pharmacology was used to determine the mechanism of action. The Traditional Chinese Medicine Inheritance Support System platform was used to investigate prescription patterns, core drugs, and optimum combinations of hypoglycemic TCMFs for AD. Results: Sixteen hypoglycemic TCMFs prolonged the PT50 (half paralysis time) of the CL4176 strain of C. elegans, reduced the percentage of worms paralyzed. The results of network pharmacology showed that prostaglandinendoperoxide synthase 2 (PTGS2) and acetylcholine esterase (AChE) are main targets of hypoglycemic TCMFs. Enriched pathway analysis showed that the cholinergic receptor-related pathway was the core pathway of hypoglycemic TCMFs. According to the "four qi and five flavors" system of TCM theory, the main pharmacological qualities were "cold" and "sweet." Through the analysis by TCMISS, we found that Huangqi-Gegen drug pair as the significant Chinese herbs of hypoglycemic TCMFs. The Huangqi-Gegen pairing had the most robust therapeutic effect when delivered at a 2:1 (v/v) ratio. It reduced the paralysis caused by 5-HT, decreased protein expression of AChE and PTGS2, and reduced AO deposition in the brain of the CL2006 strain of C. elegans.

OBJECTIVE:Shenmai injection is a classic herbal prescription, and is often recommended for the treatment of anthracycline-induced cardiotoxicity. However, the efficacy and safety of Shenmai injection for the treatment of anthracycline-induced cardiotoxicity have not been reported. MATERIALS AND METHODS:We conducted a comprehensive search of eight literature databases and two clinical trial registries, retrieving all randomized controlled trials (RCTs) related to the treatment of anthracycline-induced cardiotoxicity with Shenmai injection from the establishment of the databases to July 1, 2023. Data analysis was performed using the Meta package in RStudio and RevMan 5.4. The GRADE pro3.6.1 software was utilized for assessing the quality of evidence. RESULTS:A total of 16 RCTs including 2140 patients were included in this study. Meta-analysis showed that Shenmai injection had an advantage in improving ST-T segment changes (RR = 0.28; 95 % CI, 0.20 to 0.39; P < 0.0001) (P < 0.01), creatine kinase isoenzyme (SMD = -3.49; 95 % CI, -5.24 to -1.74; P < 0.0001), Prolonged QT interval (RR = 0.46; 95 % CI, 0.28 to 0.75; P = 0.0018), Low QRS Voltage (RR = 0.44; 95 % CI, 0.27 to 0.71; P = 0.0007), sinus tachycardia (RR = 0.41; 95 % CI, 0.28 to 0.60; P < 0.0001), atrial premature beats (RR = 0.55; 95 % CI, 0.35 to 0.87; P = 0.01), Premature Ventricular Contractions (RR = 0.39; 95 % CI, 0.26 to 0.59; P < 0.0001) and creatine kinase (SMD = -1.43; 95 % CI, -2.57 to -0.29; P < 0.0001) in patients with anthracycline-induced cardiotoxicity. advantage, which was supported by sensitivity analyses, but not in improving left ventricular ejection fraction (MD = 16.01; 95 % CI, -3.10 to 35.12; P = 0.10) and atrioventricular block (RR = 0.49; 95 % CI, 0.24 to 1.03; P = 0.06). The literature included in the study did not refer to data regarding the safety aspects of Shenmai injection, so we do not yet know the safety of Shenmai injection. The results of subgroup analyses suggested that heterogeneity was not related to the administered dose and chemotherapy regimen. The publication bias test showed no publication bias. The quality of evidence for the results ranged from "very low" to "moderate." CONCLUSION:This study suggests that Shenmai injection is effective in treating anthracycline-induced cardiotoxicity and is a potential treatment for anthracycline-induced cardiotoxicity. However, due to the poor methodological quality of the included RCTs, we recommend rigorous, high-quality, large-sample trials to confirm our findings.

Lanzhou lily (Lilium davidii var. willmottiae) is an exclusive sweet lily variety indigenous to China, which is susceptible to bulbous rot caused by fungal infection during storage. This experiment tests the pathogenicity of the pure culture isolated from the diseased tissue was confirmed in accordance with Koch's postulates, and the pathomycetes were identified based on their morphological and molecular characteristics. Furthermore, the biological characteristics of the pathogens were investigated, followed by an evaluation of the antifungal effects of three plant essential oils against them. The results showed that two strains of fungi were isolated from Lanzhou lily rot, which were identified as Fusarium oxysporum Schl. and Aspergillus sydowii (Bain. Et sart.). In addition, the pathogenicity of these two strains of fungi was demonstrated that only F. oxysporum induced rot with similar symptoms during the post-harvest storage period. The biological characteristics of F. oxysporum indicated the potato maltose agar and lily dextrose agar were identified as the most suitable media. Sucrose was determined to be the optimal carbon source, while ammonium nitrate was found to be the best nitrogen source for the growth of F. oxysporum. Mycelial growth and sporulation of F. oxysporum occurred at an optimum pH value of 6. Total darkness facilitated mycelial growth and conidial germination. The ideal temperature for growth was found to be 28°C, while relative humidity did not significantly impact mycelial growth; however, a relative humidity of 55% was most favorable for spore production. Among the three essential oils tested, cinnamon essential oil displayed superior antifungal efficacy against F. oxysporum, whereas angelica essential oil and tea tree essential oil also exhibited moderate inhibitory effects against this pathogen. This research provides valuable theoretical insights for disease control during the storage and transportation of Lanzhou lily.

阿霉素属蒽环类抗生素,作为广谱抗肿瘤药,广泛应用于临床.但阿霉素具有剂量依赖性,并呈现出明显的心脏毒性,使得临床应用受到限制.目前针对阿霉素致心脏毒性的作用机制尚未完全阐明,减少心脏毒性提高临床应用范围,成为近几年研究的热点.本文从阿霉素的心脏毒性机制、中药防治阿霉素心脏毒性两个方面进行综述,以期为阿霉素联合应用提供参考.

探讨7味药食同源中药水提取物及其联用对大肠杆菌、金黄色葡萄球菌、白色念珠菌的体外抑菌效果,并将其应用于抑菌喷雾剂.采用水提法提取药液,用纸片扩散法测得单药最低抑菌浓度(MIC)及最小杀菌浓度(MBC),同时以"棋盘法+中药互配"筛选对上述致病菌具有较强协同抑制作用的药物组合,并确定适宜的药物配伍制备抑菌喷雾剂.结果显示,7味药食同源中药对3种供试病原菌均具有不同程度的抑菌效果,五味子、金银花、牡丹皮、肉桂、白芍和山楂的抑菌作用较强,其对大肠杆菌的抑菌圈直径为12.50～26.50 mm,最低抑菌浓度(MIC)＜250.00 mg/mL,最小杀菌浓度(MBC)＜500.00 mg/mL;其中,五味子的抑菌作用最显著,对大肠杆菌、金黄色葡萄球菌、白色念珠菌的MIC分别为31.25 mg/mL、15.62 mg/mL、250.00 mg/mL.互配试验结果表明,10种不同的药物组合对3种供试菌的联合抑菌作用各不相同,牡丹皮和肉桂的配伍组合对大肠杆菌以及肉桂和五味子的配伍组合对金黄色葡萄球菌的联合抑菌指数(FICI)均≤0.50,表现为协同作用,其中肉桂和白芍、牡丹皮和白芍的配伍组合对致病菌也有协同或相加作用.因此,选择牡丹皮、肉桂、五味子、白芍4味药食同源中药制备抑菌喷雾剂.同时初步确定药食同源中药抑菌喷雾制剂的制备工艺流程为在40℃水浴中,向中药提取液中依次搅拌加入0.2％苯甲酸、1.0％吐温-80和5.0％1,2-丙二醇.多种药食同源中药具有抗菌作用,且合理的配伍可以产生协同增效的效果,为无毒副作用抗菌喷雾剂的开发奠定了基础.

目的 运用网络药理学方法探究大泻心汤治疗肺癌的作用机制.方法 通过中药系统药理学数据库与分析平台(TCMSP)获取大泻心汤中单味药的活性成分及其靶点.利用疗效药靶数据库(TTD)、Dis-GeNET数据库查找肺癌相关靶点,使用Cytoscape 3.7.2软件确定该复方治疗肺癌的关键靶标,绘制蛋白质-蛋白质相互作用(PPI)图,同时构建"中药-化合物-靶点-疾病"网络构建图.使用DAVID平台对共同靶点进行基因本体(GO)功能分析和京都基因与基因组百科全书(KEGG)信号通路富集分析,并使用Omicshare Tools进行可视化.结果 大泻心汤共筛选获得164个活性成分,与肺癌疾病靶点交集出154个共同靶点,通过筛选共同靶点得到27个关键靶点,主要为信号转导和转录活化因子3(STAT3)、丝氨酸/苏氨酸蛋白激酶1(AKT1)、丝裂原活化蛋白激酶1(MAPK1)及肿瘤抑制基因TP53等.GO功能分析显示与细胞氧化应激反应、核受体、转录因子调节等有关;KEGG信号通路富集分析得到173条信号通路,主要涉及乙型肝炎、糖尿病并发症中的AGE-RAGE信号通路、流体剪切应力与动脉粥样硬化、小细胞肺癌、胰腺癌、人T细胞白血病病毒1感染等多条信号通路.结论 大泻心汤主要通过多成分、多靶点、多通路抑制肿瘤细胞的增殖和生长,从而治疗肺癌.

目的 探究五倍子、黄芩、金银花、板蓝根、连翘、薄荷、山楂七味中药及其组方的抑菌作用.方法 使用水煎煮法提取各单味中药及其组方的活性成分;采用琼脂平板打孔法、纸片扩散法和平板培养法测定其抑菌圈直径、最小抑菌浓度(MIC)和最小杀菌浓度(MBC);设计7因素2水平的正交试验,初步确定最优抑菌配比.选择对抑菌活性影响最小的脱色方法.结果 7味中药中五倍子对金黄色葡萄球菌的抑菌作用最强,抑菌圈直径(30.3±0.81)mm;山楂对大肠埃希菌的抑菌作用最强,抑菌圈直径(17.7±1.03)mm;黄芩对白色念珠菌的抑菌作用最强,其抑菌圈直径为(14.5±1.38)mm.正交试验结果表明,连翘、山楂、板蓝根、五倍子、金银花、黄芩、薄荷按质量比为2:1:2:2:1:2:1组成的中药组合物抑菌效果最好.75％水提醇沉法脱色对抑菌作用影响小.结论 五倍子、山楂和黄芩分别对金黄色葡萄球菌、大肠埃希菌、白色念珠菌的抑菌作用最强,7味中药的配伍可以产生协同增效的效果,可使用75％水提醇沉法对药液脱色.

目的:建立LPS(脂多糖)诱导的急性肺损伤小鼠模型,探究麻杏石甘汤对急性肺损伤的保护作用及机制.方法:将C57BL/6雄性小鼠随机分为正常对照组、模型对照组、麻杏石甘汤5.4、54、108 g/kg组和哌非尼酮200 mg/kg组,每组10只,连续灌胃给予相应药物或去离子水7 d,第8 d注射LPS建立急性肺损伤模型,从肺功能检测、肺部CT检测、脏器指数、肺组织病理学检查、肺组织湿/干质量比(W/D)、血清及肺灌注洗液(BLAF)中肿瘤坏死因子α(TNF-α)、白介素1 β(IL-1 β)、IL-6含量测定、肺组织氧化应激指标变化等综合探讨麻杏石甘汤对LPS诱导的急性肺损伤小鼠的保护作用机制.结果:与正常对照组比较,模型对照组肺灌洗液和血清中TNF-α、IL-1 β、IL-6含量,肺组织病理学产生变化,肺功能指标明显改变、CT异常、肺指数显著增加,炎症因子明显增加,氧化指标明显异常,成功建立急性肺损伤模型(P＜O.05或P＜0.01);麻杏石甘汤能明显或部分改善模型小鼠肺部炎性细胞浸润,改善肺功能和肺部CT,能明显降低LPS诱导的急性肺损伤模型小鼠中肺组织的丙二醛(MDA)的含量,同时也能增强急性肺损伤小鼠肺组织中的超氧化物歧化酶(SOD)和还原型谷胱甘肽(GSH)的活力,还能降低血清和BLAF中IL-1 β、IL-6以及TNF-α等细胞炎症因子的含量,下调肺组织p38MAPK、JNK、ERK1/2、TNF-α、IL-6蛋白的表达(P＜0.05或P＜0.01).结论:麻杏石甘汤可能通过抗氧化应激、抑制相关炎症因子、调节炎症MAPK/NF-kB通路等多种途径有效预防急性肺损伤.

KRAS is a biomarker for non-small cell lung cancer-targeted therapy, but there is currently no effective KRAS-targeting medication. Realgar is an impelling anti-cancer drug, however its significance in KRAS mutant lung cancer is uncertain. According to our findings, the IC50 of H23 (KRAS mutant) cells is 2.99 times lower than that of H1650 (non-KRAS mutant) cells. Flow cytometry and the Hoechst 33258 staining assay revealed that H1650 cells treated with 4 µg/ml realgar had an apoptotic rate of 8.2%, while H23 cells had a rate of 21.46%. Accordingly, realgar was more sensitive to KRAS mutant cells. Transcriptome sequencing test indicated that there were 481 different expression genes in H23 cells treated with realgar. In H23 cells treated with realgar, mitochondria shrank, inner membrane folding was disturbed, and mitochondrial membrane potential crushed. Realgar boosted intracellular Fe2+, reactive oxygen species, malondialdehyde and glutathione levels, which were all reversed by ferroptosis inhibitor Fer-1. Realgar decreased phosphorylated p-Raf, p-ERK1/2 and increased p-p38 and p-JNK, whereas only p-Raf was abolished by Fer-1. Raf inhibitor Sorafenib accelerated the realgar-induced ferroptosis. On H23 cells treated with realgar, the expression of GPX4, SCL7A11 decreased while ACSL4 expression increased; this effect could also be amplified by Sorafenib. In conclusion, the present study indicated that realgar may induce ferroptosis by regulating the Raf, and hence plays a role in anti-KRAS mutant lung cancer.

The research status and development trend of nanotoxicology of Liliaceae medicinal plants were analyzed. In the research, the toxicology of Liliaceae medicinal plants was investigated by the preparation method of silver nanoparticles. By means of spectral curve experiment, the present situation of nanotoxicology of Liliaceae medicinal plants was analyzed, and then its subsequent development trend was analyzed. In this process, Liliaceae medicinal plants could be used effectively, which could create great economic benefits. In the application of the above scheme, the toxicological degradation of Liliaceae medicinal plants could be controlled at about 96%. The high-dose silver nanoparticles could reach 100 μM, and the silver nitrate could reach 10 or 30 μM.

目的 基于网络药理学探究敦煌平胃丸对人胃癌细胞株SGC-7901的抑制作用.方法 建立BALB/c裸鼠移植瘤模型,随机分为对照组、顺铂组、敦煌平胃丸组,每组8只,分别给予生理盐水腹腔注射、顺铂腹腔注射、敦煌平胃丸灌胃给药10 d,通过抑瘤率、瘤体形态、肿瘤细胞凋亡检测抑瘤情况.通过TCMSP、NCBI、TTD等在线数据库构建"药物-成分-靶点"网络,得到敦煌平胃丸治疗胃癌的有效成分及关键靶点,分析关键靶点的KEGG通路和GO功能.结果 与对照组比较,顺铂组、敦煌平胃丸组小鼠移植瘤体积均减小(P<0.01),肿瘤细胞凋亡率增高(P<0.01),细胞和组织异型性降低.网络药理学分析得到胃癌靶点720个,敦煌平胃丸有效成分133个,成分靶点670个,以3种互作分析方法得到敦煌平胃丸治疗胃癌的关键靶点103个,关键靶点对应的关键成分84个,KEGG通路富集得到16536条信号通路,TOP20的通路与癌症密切相关.结论 敦煌平胃丸对胃癌移植瘤具有抑制作用,网络药理学显示该复方中多种小分子通过多个关键靶点和对应的多条通路,以"多点显效,协同增效"的特点发挥抑瘤作用.

Background. Gastric adenocarcinoma (GAD) is one of the most common tumors in the world and the prognosis is still very poor. Objective. We sought to identify reliable prognostic biomarkers for the progression of GAD and the sensitivity to drug therapy. Method. The RNA sequencing data of GAD was downloaded from the Cancer Genome Atlas (TCGA) database and used for analysis. Differentially expressed, immune-related lncRNA (DEIRlncRNA) was characterized by differential analysis and correlation analysis. Univariate Cox regression analysis was used to identify DEIRlncRNA associated with prognosis. Least absolute shrinkage and selection operator (LASSO) regression analysis allowed us to determine a signature composed of eight IRlncRNAs. Based on this signature, we further performed gene set enrichment analysis (GSEA) and somatic mutation analysis to evaluate the ability of this signature to predict prognosis. Results. In total, 72 immune-related lncRNAs (DEIRlncRNAs) with prognostic value were identified. These lncRNAs were used to construct a model containing eight immune-related lncRNAs (8-IRlncRNAs). Based on this risk model, we divided GAD patients into high-risk and low-risk groups. The analysis showed that the prognosis of the two groups was different and that the high-risk group had worse overall survival (OS). Immune cell infiltration analysis showed that the proportion of memory B cells increased in the high-risk group while the proportion of macrophages M1, T cells, CD4 memory-activated cells, and T cell follicular helpers decreased. GSEA results showed that 8-IRlncRNA was significantly enriched in tumorigenesis pathways such as myc. The results of somatic mutation analysis showed that the CDH1 gene was significantly mutated in the high-risk group. Conclusion. A prognostic signature of 8-IRlncRNAs in GAD was established and this signature was able to predict the prognosis of GAD patients.

Acute pancreatitis (AP), as a common cause of clinical acute abdomen, often leads to multi-organ damage. In the process of severe AP, the lungs and intestines are the most easily affected organs aside the pancreas. These organ damages occur in succession. Notably, lung and intestinal injuries are closely linked. Damage to ML, which transports immune cells, intestinal fluid, chyle, and toxic components (including toxins, trypsin, and activated cytokines to the systemic circulation in AP) may be connected to AP. This process can lead to the pathological changes of hyperosmotic edema of the lung, an increase in alveolar fluid level, destruction of the intestinal mucosal structure, and impairment of intestinal mucosal permeability. The underlying mechanisms of the correlation between lung and intestinal injuries are inflammatory response, oxidative stress, and endocrine hormone secretion disorders. The main signaling pathways of lung and intestinal injuries are TNF-α, HMGB1-mediated inflammation amplification effect of NF-κB signal pathway, Nrf2/ARE oxidative stress response signaling pathway, and IL-6-mediated JAK2/STAT3 signaling pathway. These pathways exert anti-inflammatory response and anti-oxidative stress, inhibit cell proliferation, and promote apoptosis. The interaction is consistent with the traditional Chinese medicine theory of the lung being connected with the large intestine (fei yu da chang xiang biao li in Chinese). This review sought to explore intersecting mechanisms of lung and intestinal injuries in AP to develop new treatment strategies.