Anti-melanoma action of small molecular peptides derived from Brucea javanica(L.)Merr.globulin in vitro

Objective:The morbidity of malignant melanoma keeps increasing annually.It has high risks of metastasis,drug resistance,and poor prognosis in clinics.Moreover,the available medicines used commonly,such as dacarbazine,temozolomide,the v-Raf murine sarcoma viral oncogene homolog B1(BRAF)inhibitor vemurafenib,and the programmed cell death protein 1 inhibitor pembrolizumab,have some limitations at some extent.Therefore,a more effective therapeutic strategy is still urgently necessary.Methods:In this study,Brucea javanica(L.)Merr.globulins were hydrolyzed with pepsin,then ultra-filtrated to collect small molecular peptides(≤3 kDa).The peptides were then analyzed by antiproliferative assay,cell-cycle distribution,apoptosis assay,and in vitro wound-scratch assay.Finally,western blotting was conducted to elucidate the underlying anti-melanoma mechanism.Results:The small molecular peptide from B.javanica significantly inhibited malignant melanoma cell proliferation with the IC_(50) of 2.72 mg/mL for 72 h.Further analysis indicated that B.javanica peptides arrested cell cycle at the S and G2/M phases and induced apoptosis by upregulating p21,p53,Bax,caspase-3,and cleaved PARP while downregulating Bcl-2 expression.The inhibitory migration effects were also confirmed by wound-healing assay.Conclusion:The small molecular biopeptides from B.javanica may be a promising bioactive agent candidate for melanoma treatment.

Brucea javanica oil inhibits proliferation of hepatocellular carcinoma cells and induces apoptosis via the PI3K/AKT pathway

Background:Brucea javanica oil(BJO),distributed primarily in Southeast Asia,has long been utilized as a therapeutic agent for treating malignancies.However,its anticancer mechanisms are not clearly understood.The objective of this study was to examine the mechanisms underlying its treatment of hepatocellular carcinoma cells.Methods:CCK8 assay was used to evaluate cell viability.Hoechst33342 staining and flow cytometry analyses were used to examine apoptosis.Mito-Tracker Red CMXRos kit was used to measure the membrane potential of mitochondria.ATP assay kit was used to evaluate ATP levels.Western blots were used to assess the presence of AKT,adenosine monophosphate-activated protein kinase,Caspase3,Caspase9,Bax,and Bcl-2.Results:BJO inhibited the proliferation of hepatocellular carcinoma cells HepG2 in a time-and dose-dependent manner.It induced apoptosis,with the percentage of cells treated with 50–150μg/mL BJO increasing from 8.01%to 28.02%in a concentration-dependent manner(P<0.05,when 50μg/mL of BJO group compared with the control group;P<0.001,when 100 or 150μg/mL of BJO group compared with the control group).After exposed to BJO,the expression of C-caspase3,C-caspase9 and Bax upregulated while that of Bcl-2 downregulated.BJO suppressed the PI3K/AKT pathway and promoted phosphorylation of adenosine monophosphate-activated protein kinase,while repressing the phosphorylation of mechanistic target of rapamycin.Compared with treatment by BJO alone,the PI3K/AKT agonist 740Y-P increased the survival rate of HepG2 cells(P<0.01)and attenuated the inhibitory effect of BJO on cell apoptosis(P<0.05).Conclusion:BJO is capable of inhibiting proliferation of HepG2 cells and inducing apoptosis via the PI3K/AKT pathway.

Brucea javanica oil emulsion improves the effect of radiotherapy on esophageal cancer cells by inhibiting cyclin D1-CDK4/6 axis

BACKGROUND Esophageal cancer is one of the most common cancers around the world, and it has high incidence and mortality rates. The conventional therapy for esophageal cancer is radiotherapy, although its effect is highly limited by the resistance of esophageal cancer cells. Thus, strong radiosensitizers can be very crucial during radiotherapy against esophageal cancer. Brucea javanica oil emulsion (BJOE) is a widely used drug against various cancers, such as liver, colon, and ovarian cancer. However, its anti-cancer effect and mechanism and the use of BJOE as a radiosensitizer have not been explored in esophageal cancer. AIM To evaluate the anti-cancer effect and mechanism of BJOE and explore the potential use of BJOE as a radiosensitizer during radiotherapy. METHODS The inhibitory effect of BJOE and its enhancement function with radiation on cell viability were examined with the calculated half-maximal effective concentration and half-maximal lethal concentration. The influence of BJOE on cell migration and invasion were measured with EC109 and JAR cells by wound-healing and transwell assay. Clonogenesis and apoptotic rate, which was measured by Hoechst staining, were investigated to confirm its enhancement function with radiation. To investigate the molecular pathway underlying the effect of BJOE, the expressions of several apoptosis- and cycle-related proteins was detected by western blotting.cell lines more than normal cell lines, and it markedly reduced migration and invasion in esophageal cancer cells (EC109 and JAR). Moreover, it promoted cell apoptosis and enhanced the effect of radiotherapy against esophageal cancerous cells. In the viability test, the values of half-maximal effective concentration and half-maximal lethal concentration were reduced. Compared to the control, only around 1/5 colonies formed when using BJOE and radiation together in the clonogenic assay. The apoptotic rate in EC109 was obviously promoted when BJOE was added during radiotherapy. Our study suggests that the expression of the apoptosis-proteins Bax and p21 were increased, while the expression of Bcl-2 was stable. Further detection of downstream proteins revealed that the expression of cyclin D1 and cyclin-dependent kinase 4/6 were significantly decreased. CONCLUSION BJOE has a strong anti-cancer effect on esophageal cancer and can be used as a radiosensitizer to promote apoptosis in cancerous esophageal cells via the cyclin D1-cyclin-dependent kinase 4/6 axis.

Activity of Brucea javanica oil emulsion against gastric ulcers in rodents

The present study aims to investigate the gastroprotective effect of Brucea javanica oil emulsion(BJOE) in animals. Gastroprotective potential of BJOE was studied on absolute ethanol,aspirin, reserpine and restraint plus water immersion-induced gastric ulcers in mice as well as glacial acetic acid(GAA) and pyloric ligation(PL)-induced gastric ulcers in rats. Except for ulcer scores, total acidity as well as pepsin activity as for the PL-induced gastric ulcer model and ulcer incidence as for the GAA-induced gastric ulcer model were also determined. Histopathological evaluation as for aspirin, reserpine, PL-induced models was conducted. Results showed that BJOE significantly(P < 0.05) reduced ulcer index in the mouse and rat models in a dose-dependent manner. It had significant(P < 0.05) suppressive effect on total activity of gastric juice as well in PL-induced model. Histopathological examination for the stomach samples confirmed the findings in the aspirin, reserpine or PLinduced gastric lesion models, which showed relatively complete mucosa structure and less inflammation. It is concluded that BJOE could be effective on gastric ulcer in rodents and its gastroprotective activity might be related to antioxidant, anti-inflammatory ability and promote gastric mucus secreted. The results may provide beneficial basis for increasing BJOE's clinical indication in future.

Formulation and characterization of brucea javanica oil microemulsion

Objective This study engaged in investigation of optimal formulation,characteristics analysis of Brucea javanica oil microemulsion(BJOM) in order to address safety concerns and make recommendations for improvements in BJOM safety during clinical use in vivo.Methods Pseudo-ternary phase diagram techniques were used to determine the appropriate ratio of surfactant,cosurfactant,and oil phases.Subsequent stability testing of BJOM was performed by dilution,centrifugation,and accelerated stability testing.The results were expounded through additional assessment utilizing the classical thermostat method to establish the shelf life of the material.These results were utilized to evaluate the safety of BJOM by haemolytic,irritative and allergic testing in vitro.In addition,the cytotoxicity of BJOM was examined using the tetrazolium salt 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide(MTT),with particular emphasis given to potential uses in cancer treatment.Results The most suitable method of preparation for BJOM was found to be a one to one ratio(Km 1∶ 1) of Solutol HS15 surfactant matched with sorbitol cosurfactant in the ratio.The microemulsion droplets of BJOM possessed a spherical shape,uniform size,and average diameter of 23.8nm.The expiration date of BJOM was found to be 568d.The safety study demonstrated no haemolysis activity at the experimental BJOM concentrations;however,mild haemolysis was observed at higher concentrations of Brucea javanica oil emulsion(BJOE),a common commercially available product.Irritation observed upon BIOM treatment can be primarily attributed to Brucea javanica oil(BJO) with little influence of BJOM excipients.In addition,BJOM caused no observed hypersensitivity or other visible allergic reactions in guinea pigs.The anticancer activity curves of BJOM and BJOE demonstrate that both BJOM and BJOE inhibit Hela cells,with BIOM demonstrating significantly more dramatic anticancer activity.Conclusion An optimal formulation of BJOM superior to commercially available products and safe for medical application such as intravenous injection has been outlined along with its anticancer activity rating.

Preparation and evaluation of paclitaxel and Brucea javanica oil core-matched nanoemulsions to treat cancer in vitro and in vivo

Objective: Developed the core-matched nanoemulsions(CMNEs) to co-delivery paclitaxel-oleic acid(PTXOA) prodrug and Brucea javanica oil(BJO) for increasing the antitumor effect.Methods: Antitumor effects and mechanism of PTX-OA/BJO CMNEs that the combination therapy which based on core-matched technology(CMT) were evaluated in vitro and in vivo.Results: The PTX-OA/BJO CMNEs were of nanoscale particle size(108.7 ± 2.3) nm and with entrapment efficiency of >95%. The PTX-OA/BJO CMNEs displayed concentration and time-dependent cytotoxicity against HepG-2 cells and increased G2/M phase block. More importantly, a significant reduction of the tumor volume with no obvious toxicity was observed in nude mice model following administration of PTX-OA/BJO CMNEs compared with the control treated with normal saline(P < 0.05), which suggested the excellent efficacy in vivo. It was further found that the enhanced effectiveness of PTX-OA/BJO CMNEs were associated with the ability of inducing apoptosis of the tumor cells, as well as obviously inhibiting tumor cell proliferation and the activity of TOPOⅡ.Conclusion: Co-encapsulation of two drugs with different mechanisms allows simultaneous interruption of diverse anticancer pathways, resulting in increased therapeutic response and lower toxicity.

Brusatol:A potential anti-tumor quassinoid from Brucea javanica

Brusatol,a triterpene lactone compound mainly from Brucea javanica,sensitizes a broad spectrum of cancer cells.It is known as a specific inhibitor of nuclear factor-erythroid 2-related factor 2(Nrf2)pathway.In this review,we provide a comprehensive overview on the antitumor effect and molecular mechanisms of brusatol in vitro and in vivo.This review also covers pharmacokinetics studies,modification of dosages forms of brusatol.Increasing evidences have validated the value of brusatol as a chemotherapeutic agent in cancers,which may contribute to drug development and clinical application.

Research of Brucea javanica against Cancer

Brucea javanica, a Chinese herbal medicine, combined with conventional anticancer modalities, has been widely used for treatment of various cancers. Based on researches over the last decades, authors briefly summarized its active constituents, molecular mechanisms and clinical application for cancer treatment.

Formulation development and evaluation of gastroretentive floating beads with Brucea javanica oil using ionotropic gelation technology

In the present study, a gastric retention floating system for Brucea javanica oil, composed of alginate and carrageenan, was prepared using ionotropic gelation. Parameters for floatability, drug load, encapsulation efficiency, bead morphology, in vitro release, and in vivo gastric retention were evaluated. The optimized formulation via Box–Behnken design consisted of 1.7% alginate(W/V), 1.02% carrageenan(W/V), 1.4% CaCO_3(W/V), and a gelling bath of pH 0.8. The alginate–carrageenan–Brucea javanica oil beads had a porous structure and exhibited up to 24 h of in vitro floatability with a load capacity of 45%–55% and an encapsulation efficiency of 70%–80%. A 6-h sustained release was observed in vitro. The beads had a prolonged gastric retention(> 60% at 6 h) in fasted rats, compared to non-floating beads(15% at 6 h), as measured by gamma scintigraphy with single-photon emission tomography/computed tomography(SPET/CT). In conclusion, the alginate–carrageenan–Brucea javanica oil system showed enhanced oil encapsulation efficiency, excellent floating and gastric retention abilities, and a favorable release behavior.

Seed oil of Brucea javanica induces apoptosis through the PI3K/Akt signaling pathway in acute lymphocytic leukemia Jurkat cells

Brucea javanica oil emulsion(BJOE)has been used to treat tumor in China for more than 40 years.However,its components and effectiveness in the treatment of acute lymphocytic leukemia(ALL)and its mechanism of anti-cancer activity remain unknown.In the current study,high-performance liquid chromatography-evaporative light scattering detector(HPLC-ELSD)was used to analyze the components of BJOE.Then,the anti-leukemia effects of BJOE were examined both in vitro and in vivo using ALL Jurkat cells and the p388 mouse leukemia transplant model,respectively.The primary ALL leukemia cells were also used to confirm the antileukemia effects of BJOE.The apoptotic-related results indicated that BJOE induced apoptosis in Jurkat cells and were suggestive of intrinsic apoptotic induction.Moreover,BJOE inhibited Akt(protein kinase B)activation and upregulated its downstream targets p53 and Fox O1(forkhead box gene,group O-1)to initiate apoptosis.The activation of GSK3βwas also involved.Our findings demonstrate that BJOE has anti-leukemia effects on ALL cells and can induce apoptosis in Jurkat cells through the phosphoinositide3-kinase(PI3 K)/Akt signaling pathway.

The aqueous extract of brucea javanica reduces tumorigenicity of human lung cancer tumorspheres

Aim:Therapy to overcome drug resistance by modulating epidermal growth factor receptor(EGFR)is a viable approach to suppress the proliferation of human non-small cell lung cancer(NSCLC)cells.A previous study demonstrated that the seeds of an aqueous Brucea javanica(BJ)(L.)Merr(Simaroubaceae)extract containing quassinoid mixtures effectively inhibited the growth and alleviated tumorigenesis in H1975 cells of NSCLC by targeting T790M/L858R EGFR.This study aimed to further determine whether the aqueous BJ extract affects the enriched H1975 spheroids in suspension culture and mouse xenograft tumor models.Methods:The spheroids of NSCLC adenocarcinoma H1975 cells were enriched in a serum-free media.The growth rate of sphere propagation by aqueous BJ extract was determined in suspended culture and in colony-formation assay.BJ extract was fed orally to nude mice bearing xenograft tumors.The resected tumors were analyzed by hematoxylin and eosin staining,terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay,and proliferating cell nuclear antigen assessment.Various markers were used to determine the pluripotency of tumors from mice treated with different concentrations of BJ extract.Results:BJ extract was demonstrated to be effective against the propagation of the enriched spheroids.In animal models,oral administration of the aqueous BJ extract reduced spheroid tumorigenicity.The alleviated growth of the established xenograft tumors can be attributed to the reduced drug resistance and induced apoptosis without distinct adverse effects.More evidence supports activated apoptotic death attenuated spheroid stemness of tumors.Conclusion:As an effective treatment regime to assuage lung cancer,the indigenous BJ extract promises to obliterate drug resistance and the growth of cancer stem cell tumors from NSCLC cells harboring T790M/L858R EGFR.

鸦胆子结合吡柔比星对膀胱癌细胞作用的影响

目的探究鸦胆子结合吡柔比星对膀胱癌细胞的作用。方法选取2023年4—5月期间黑龙江省医院泌尿科1株人BIU-87膀胱癌细胞株为研究对象,细胞培养后,将其接种于96孔板中,以随机数表法分为5组,每组细胞均进行3个平行样本,每个样本细胞均设置5个复孔(每组共计15个样本量),将5组细胞以不同浓度鸦胆子油乳(0、5、10、20、30 mL/L)与吡柔比星(5μmol/L)联合作用,分析不同浓度鸦胆子油乳对膀胱癌细胞增殖抑制作用、细胞凋亡及细胞周期影响,并检测联合用药对核因子κB(Nuclear FactorκB,NF-κB)影响、对细胞中三磷酸腺苷(AdenosineTriphosphate,ATP)结合转运蛋白G家族成员2(ATP-bindingCassette TransporerG2,ABCG2)表达情况影响。结果鸦胆子油乳浓度升高,BIU-87细胞增殖抑制率、坏死率、凋亡率逐渐升高,差异有统计学意义(P均<0.05);鸦胆子油乳浓度为5 mL/L时细胞增殖抑制率、细胞坏死率显著提升,浓度≥10 mL后,细胞凋亡率显著提升,差异有统计学意义(P均<0.05);随鸦胆子油乳浓度升高,BIU-87细胞中S期细胞占比降低,C0/C1期细胞占比升高,差异有统计学意义(P均<0.05);随鸦胆子油乳浓度升高,细胞质中NF-κB表达量逐渐下降,细胞核中NF-κB表达量逐渐升高,细胞膜表面ABCG2表达量下降,差异有统计学意义(P均<0.05)。结论鸦胆子油乳结合吡柔比星,可抑制BIU-87膀胱细胞株增殖,低浓度可促进细胞坏死,高浓度可促进细胞凋亡,并促进NF-κB从细胞质转入细胞核中,抑制ABCG2表达,其效果均存在剂量依赖性。

鸦胆子油乳对肺癌A549细胞顺铂化疗的增敏作用及其机制

目的观察鸦胆子油乳对肺癌A549细胞顺铂化疗的增敏作用并分析其机制。方法体外培养人肺癌细胞A549,MTT法检测鸦胆子油乳、顺铂对细胞生长的抑制率,计算鸦胆子油乳、顺铂对细胞的半数抑制浓度(IC_(50)),观察不同浓度(2.44、9.77、78.12μg/mL)鸦胆子油乳对顺铂IC_(50)的影响。将A549细胞分为对照组、鸦胆子油乳组、顺铂组及鸦胆子油乳+顺铂组,对照组不做处理正常培养细胞,鸦胆子油乳组、顺铂组及鸦胆子油乳+顺铂组分别给予鸦胆子油乳单药、顺铂单药、鸦胆子油乳及顺铂联合处理。采用荧光显微镜观察细胞形态及生长情况,流式细胞术检测细胞周期及细胞凋亡率,二氯荧光素二乙酸酯荧光探针染色检测细胞内ROS水平。结果顺铂IC_(50)随着鸦胆子油乳处理浓度的增高而下降(P均<0.05)。对照组细胞生长较好,细胞数量较多且形状为正常生长状态;顺铂组及鸦胆子油乳组细胞数量较对照组均减少,可见少量碎片;鸦胆子油乳+顺铂组细胞生长受抑制较明显,细胞数量最少,细胞形状不规则且细胞碎片增多。G_(0)/G_(1)期细胞比例鸦胆子油乳+顺铂组>顺铂组、鸦胆子油乳组>对照组,细胞凋亡率鸦胆子油乳+顺铂组>鸦胆子油乳组、顺铂组>对照组,细胞内ROS水平鸦胆子油乳+顺铂组>鸦胆子油乳组、顺铂组>对照组(P均<0.05)。结论鸦胆子油乳能够增加肺癌A549细胞对顺铂化疗的敏感性,其机制可能与阻滞肿瘤细胞于G_(0)/G_(1)期、增加活性氧产生从而促进细胞凋亡有关。

基于meta分析的鸦胆子油乳注射液联合长春瑞滨联合顺铂/卡铂方案治疗非小细胞肺癌临床效果和安全性

目的系统评价鸦胆子油乳注射液联合长春瑞滨联合顺铂/卡铂(NP)方案化疗治疗非小细胞肺癌(NSCLC)的临床疗效和安全性。方法检索中国知网、SinoMed、VIP、万方数据库、the Cochrane Library、PubMed、Embase数据库,搜索有关鸦胆子油乳注射液联合NP化疗治疗NSCLC的随机对照试验,检索时限均为从建库至2023年5月22日,由2名研究者独立筛选文献,提取资料并评价纳入研究的偏倚风险后,采用RevMan 5.4.1及Stata 15.1软件进行meta分析和发表偏倚检验。结果共纳入12项随机对照试验,累计801例患者。Meta分析结果显示,对比仅使用NP化疗方案,鸦胆子油乳注射液联合NP方案化疗治疗NSCLC可提高临床受益率(RR=2.00,95%CI=1.34~2.98,P=0.0006),症状总改善率(RR=1.53,95%CI=1.19~1.96,P=0.0009)和生活质量改善率(RR=2.58,95%CI=1.95~3.41,P<0.00001),降低患者白细胞减少发生率(RR=0.73,95%CI=0.62~0.86,P<0.0001)。结论联合用药方案相较于单用NP化疗方案疗效更佳,且可提高患者临床受益率、症状总改善率,改善患者生活质量,增强患者免疫功能。但本研究结论仍需未来多中心、大样本随机盲法试验数据的支持。

鸦胆子油乳注射液使用情况及合理性分析

目的 通过泰州市人民医院鸦胆子油乳注射剂使用情况的分析,加强该药在临床的合理使用,确保用药安全。方法 选取我院2022年度使用鸦胆子油乳注射液进行治疗的798例患者,分析该药治疗的肿瘤类型、不同科室使用情况、不良反应发生情况。结果入选的798例患者中,男性患者527例,女性271例;年龄29~92岁,平均年龄66.36±10.92岁。肿瘤类型最多的为食管恶性肿瘤,共计131例(16.42%),其次为肝脏恶性肿瘤与肺恶性肿瘤,分别为118例(14.79%)和116例(14.54%)。鸦胆子油乳注射液用量最大的科室胃肿瘤科,共有370例(46.37%),其次为消化内科病房与肝病科病房,分别有144例(18.05%)和102例(12.78%)。全部患者中,共出现6例不良反应,均为轻微不良反应。结论 鸦胆子油乳注射液在临床使用过程中,应严格按照适应症用药,同时应关注患者不良反应发生情况,确保临床用药安全。

鸦胆子油乳联合放疗对中老年食管癌患者血清肿瘤标志物及生活质量的影响

目的探讨鸦胆子油乳联合放疗在中老年食管癌患者中的疗效。方法选取2019年1月至2022年12月南通市通州区人民医院收治的96例中老年食管癌患者为研究对象,按照随机数字表法分为对照组与观察组,各48例。对照组实施放疗,观察组在对照组基础上加用鸦胆子油乳治疗。比较两组患者血清肿瘤标志物、临床疗效、生活质量及不良反应。结果观察组患者治疗后血清肿瘤标志物中的糖类抗原199(CA199)、糖类抗原125(CA125)及癌胚抗原(CEA)水平均低于对照组,差异有统计学意义(P<0.05);观察组患者疾病控制率高于对照组,差异有统计学意义(P<0.05);观察组患者治疗后生活质量综合评定问卷(GQOLI-74)中各维度评分均高于对照组,差异有统计学意义(P<0.05);观察组患者不良反应总发生率低于对照组,差异有统计学意义(P<0.05)。结论针对中老年食管癌患者实施鸦胆子油乳联合放疗,能够降低患者血清肿瘤标志物水平,获得较好的疾病控制效果,还可减少不良反应的发生,提升生活质量。

鸦胆子油乳注射液联合化疗治疗非小细胞肺癌有效性和安全性的系统评价和Meta分析

目的:本文旨在系统评价鸦胆子油乳注射液联合化疗治疗非小细胞肺癌的有效性和安全性。方法:检索PubMed、Embase、中国生物医学文献数据库(CBM)、中国知网(CNKI)、万方等中外数据库建库至2023年3月以来关于鸦胆子油乳注射液联合化疗治疗非小细胞肺癌的文章。本项研究的主要结局是临床收益率(生活质量)、有效率和药物不良反应。采用Cochrane标准进行评价,运用RevMan 5.4软件进行统计分析。结果:纳入16项研究进行Meta分析,共1423例受试者(观察组717例,对照组706例),临床收益率Meta分析结果显示:与对照组比较,观察组患者的临床收益率优于对照组,差异有统计学意义[RR=1.16,95%CI(1.06,1.27),Z=3.15,P=0.002];有效率Meta分析结果显示:观察组有效率高于对照组,差异有统计学意义[RR=1.28,95%CI(1.14,1.43),Z=4.19,P<0.0001];安全性Meta分析结果显示:观察组不良反应发生率低于对照组,差异有统计学意义[RR=0.56,95%CI(0.43,0.73),Z=4.23,P<0.0001]。结论:与单纯应用化疗药物相比,鸦胆子油乳注射液联合化疗其在抗肿瘤有效性和安全性方面有优势,提高临床收益率,降低不良反应,值得临床应用并进一步探讨。

鸦胆子油乳联合调强放疗对喉癌治疗效果、放疗副作用及血Treg/Th17细胞因子水平的影响

目的:研究鸦胆子油乳联合调强放疗对喉癌治疗效果、放疗副作用、血调节性T细胞/辅助性T细胞17(Treg/Th17)细胞因子水平的影响,为临床提供参考。方法:选择2021年1月—2022年7月商丘市第一人民医院收治的126例喉癌患者作为研究对象,采用随机数表法分为对照组和观察组,每组各63例。对照组采用调强放疗治疗,观察组采用鸦胆子油乳联合调强放疗治疗。比较两组患者临床疗效、治疗前及治疗21 d后血清Treg/Th17相关细胞因子[白细胞介素(IL-6)、IL-17、IL-23、转化生长因子-β (TGF-β)]水平、血清细胞角蛋白19片段抗原21-1 (CYFRA21-1)、鳞状细胞癌相关抗原(SCC)、水通道蛋白-1 (AQP-1)、斯钙素-1 (STC-1)水平,卡氏评分(KPS)及放疗副作用。结果:观察组临床总有效率高于对照组,差异有统计学意义(χ^(2)=5.420,P<0.05);治疗21 d后,观察组血清IL-6、IL-17、IL-23、TGF-β水平低于对照组,差异有统计学意义(t=5.211、17.611、7.748、9.482,P<0.05);治疗21 d后,观察组血清CYFRA21-1、SCC、AQP-1、STC-1水平低于对照组,差异有统计学意义(t=10.299、5.663、9.091、7.389,P<0.05);治疗21 d后观察组KPS评分高于对照组(t=13.674,P<0.05);观察组放疗副作用低于对照组,差异有统计学意义(χ^(2)=4.203、4.881、4.308、5.143,P<0.05)。结论:采用鸦胆子油乳与调强放疗联合治疗喉癌患者可获得更好的临床疗效,能进一步下调血清Treg/Th17细胞因子水平,提高患者体能状态,有效缓解毒副反应。

鸦胆子油乳注射液联合化疗治疗非小细胞肺癌的效果及对患者免疫功能的影响

目的探讨鸦胆子油乳注射液联合化疗治疗非小细胞肺癌的效果。方法方便选取2021年11月—2023年10月淮安八十二医院收治的96例非小细胞肺癌患者为研究对象,采用随机数表法分为对照组(48例化疗治疗)和观察组(48例化疗联合鸦胆子油乳注射液治疗),对比两组患者临床效果、免疫功能及不良反应发生率。结果治疗后,观察组治疗总有效率、CD3^(+)、CD4^(+)、CD4^(+)/CD8^(+)水平均高于对照组,CD8^(+)水平及不良反应发生率低于对照组,差异有统计学意义(P均<0.05)。结论采用化疗联合鸦胆子油乳注射液治疗非小细胞肺癌,可取得较佳的效果,能够调节患者免疫能力并降低不良反应发生率。

鸦胆子油乳剂对食管鳞状细胞癌TE-1细胞增殖、凋亡和自噬的影响及其可能的机制

目的:探讨鸦胆子油乳剂(BJOE)对食管鳞状细胞癌TE-1细胞增殖、凋亡和自噬的影响及其可能的机制。方法:按干预措施的不同,将TE-1细胞分为对照组、RAPA(自噬激动剂)组、740Y-P(PI3K激活剂)组、BJOE组、BJOE+RAPA组和BJOE+740Y-P组。采用FCM、克隆形成、Transwell实验检测细胞凋亡、增殖、迁移和侵袭能力,qPCR法检测细胞中PI3K、Akt、mTOR、LC3Ⅰ、LC3Ⅱ、p62、Beclin 1、caspase-3的mRNA表达,WB法检测PI3K、Akt、mTOR及其磷酸化、LC3Ⅱ/Ⅰ、p62、Beclin 1、caspase-3的蛋白表达。结果:与对照组比较,RAPA组和BJOE组细胞凋亡率均显著升高(均P<0.01),细胞克隆形成率、迁移和侵袭能力均显著降低(均P<0.01),细胞中PI3K、Akt、mTOR的mRNA和蛋白磷酸化水平均显著降低(均P<0.05),p62的mRNA和蛋白水平显著降低(均P<0.01),LC3Ⅱ/Ⅰ、Beclin 1和caspase-3的mRNA和蛋白水平显著升高(均P<0.05),740Y-P组的结果则相反(均P<0.05);与RAPA组或740Y-P组比较,BJOE+RAPA组或BJOE+740Y-P组细胞凋亡率显著升高(均P<0.01),克隆形成率、细胞侵袭和迁移能力显著降低(均P<0.01),PI3K、Akt、mTOR的mRNA和蛋白磷酸化水平均显著降低(均P<0.05),p62的mRNA和蛋白水平均显著降低(均P<0.05),LC3Ⅱ/Ⅰ、Beclin 1和caspase-3 mRNA和蛋白水平显著升高(均P<0.05)。结论:BJOE显著抑制TE-1细胞增殖、迁移、侵袭并促进细胞凋亡与自噬,其机制可能与抑制PI3K/Akt/mTOR信号通路的激活有关。