白细胞介素-2联合环磷酰胺对乳腺癌荷瘤小鼠调节性T细胞的影响

目的：调节性T细胞（Regulatory T cells,Treg）被认为能够抑制抗肿瘤免疫反应,从而促进肿瘤生长。环磷酰胺（Cyclophosphamide,CTX）是个常规化疗药物,现在更多的注意力集中在其小剂量应用时可以删除Treg。了解小剂量环磷酰胺联合白细胞介素-2（Interleukin-2,IL-2）对4T1Balb/c乳腺癌荷瘤小鼠调节性T细胞的影响及其抗肿瘤效果。方法：通过皮下接种4T1乳腺癌细胞建立乳腺癌Balb/c荷瘤小鼠模型;20只荷瘤小鼠随机分为IL-2＋NS组、PBS＋CTX组、IL-2＋CTX组及PBS＋NS组,在种瘤第10天开始对荷瘤小鼠分别经腹腔按方案给药。在种瘤后第16天人道处死小鼠,采用流式细胞术检测小鼠脾脏中CD4＋CD25＋调节性T细胞数量,应用ELISA法检测血清干扰素-γ浓度,电子称称量肿瘤重量。结果：与对照组相比,在应用IL-2后,荷瘤小鼠脾脏CD4＋CD25＋/CD4＋比值增加,在应用IL-2的同时使用小剂量CTX可减少CD4＋CD25＋/CD4＋的比值;单次及联合用药均可提高血清INF-γ浓度;联合用药可减少肿瘤重量。结论：小剂量CTX可以减少由使用IL-2所增加的Treg数量,促进抗肿瘤免疫,提高IL-2的抗瘤效果,从而抑制肿瘤生长。该研究可能为乳腺癌的临床治疗提供一种有效的方法。     

心理干预对非小细胞肺癌患者免疫功能及心理状态的临床研究

目的：研究心理干预对非小细胞肺癌患者免疫功能及心理状态的影响。方法：70例NSCLC患者随机分为治疗组（Tl=36）和阳性对照组（n=34）,另设正常对照组（n=30）,治疗组进行心理干预,阳性对照组和正常对照组不给予干预,30天后,计算患者的EORTCQLQ—C30积分并测定T细胞亚群CD3＋、CD4＋、CD8＋、CD4＋／CD8＋指标。结果：治疗组患者干预后的生存质量（一般情况、躯体功能、社会功能等）及CD3＋、CD4＋、CD8＋含量较干预前均有差异（P〈0．01或P〈0．05）,治疗组患者干预后的生存质量及CD3＋、CD4＋、CD8＋含量较阳性对照组干预后均有差异（P〈0．01或P〈0．05）。结论：心理干预对非小细胞肺癌患者的心理状态有积极作用,同时能提高患者的免疫力。     

DC-CIK联合化疗治疗晚期非小细胞肺癌的疗效及对免疫功能的影响

目的:研究树突细胞-细胞因子诱导杀伤细胞(DC-CIK)免疫疗法联合化疗治疗晚期非小细胞肺癌(NSCLC)的疗效及对免疫功能的影响。方法:选取2014年1月至2015年12月就诊于我院的60例Ⅲb~Ⅳ晚期NSCLC患者,采用随机数字表法分为联合组和化疗组各30例。联合组采用DC-CIK免疫疗法联合化疗(顺铂+吉西他滨),1个月为一个周期。化疗组仅进行单纯化疗,1个月为一个周期。比较两组患者近期疗效、无进展生存期(PFS)、总生存期(OS)、免疫功能、生活质量以及不良反应。结果:联合组DCR显著高于化疗组(P0.05),联合组的中位PFS高于化疗组(P0.05)。联合组治疗后外周血中的CD3+、CD3+CD4+和NK细胞较治疗前显著上升(P0.05),CD3+CD8+细胞较治疗前显著下降(P0.05),且治疗后联合组的CD3+、CD3+CD4+和NK细胞较化疗组显著上升(P0.05),CD3+CD8+细胞较化疗组显著降低(P0.05)。联合组疲乏、疼痛、食欲不振、睡眠障碍发生率低于化疗组(P0.05)。联合组白细胞减少率、血小板减少率显著低于化疗组(P0.05)。结论:DC-CIK联合化疗治疗NSCLC患者的疗效显著,可提高DCR,延长患者的PFS,提高患者的免疫功能和生活质量,减少不良反应。     

放射治疗联合参一胶囊治疗Ⅲ期非小细胞肺癌的临床研究

目的：探讨适形放射治疗联合参一胶囊在Ⅲ期非小细胞肺癌治疗中的临床疗效。方法：选取本院自2011 年4 月至2014 年6 月经病理及影像学资料明确证实的Ⅲ期非小细胞肺癌患者60 例，随机分为两组，即对照组和治疗组。对照组行单纯适形放射治 疗；治疗组在适形放射治疗的同时，给予口服参一胶囊8 周。治疗期间观察患者有无乏力症状，定期行血液学检查，完成治疗后4 周行胸部CT检查。结果：治疗组出现不同程度乏力的患者数明显少于对照组，差异显著，具有统计学意义(P<0.05)；定期血常规检 验，治疗组出现白细胞、血红蛋白减低的患者比率明显低于对照组，差异具有统计学意义(P<0.05)；两组近期治疗效果相近，差异 无统计学意义(P>0.05)。结论：放射治疗联合参一胶囊治疗可以改善患者乏力状况，降低放射治疗引起的血液不良反应的发生几 率。     

自体CAPRI细胞联合化疗治疗晚期非小细胞肺癌的临床疗效评价

目的:探讨自体CAPRI细胞联合化疗治疗晚期非小细胞肺癌的临床疗效的临床疗效。方法:选择50例晚期非小细胞肺癌患者进行分析,随机分为实验组与对照组,分别是生物治疗联合化疗组和单纯化疗组,每组25例病人。比较生物治疗联合化疗组与单纯化疗对照组患者的生存率。进行生存分析。结果:联合治疗组的OS和PFS都高于对照组。结论:自体CAPRI细胞联合化疗能够延长晚期非小细胞肺癌患者的生存期,提高患者的生存率和生活质量。     

非霍奇金淋巴瘤患者外周血中CD4＋CD25＋调节性T细胞亚群变化初探

目的：检测非霍奇金淋巴瘤（non—Hodgkin’s lymphoma,NHL）患者外周血中CD4＋CD25＋调节性T细胞（CD4＋CD25＋regulatoryTcell,Treg）的改变,探讨Treg与NHL的相关性。方法：病例组（n=60）为本院收治的初诊NHL患者,对照组（n=60）为本院健康体检者,用流式细胞技术联合标记CD4、CD25检测对照组及病例组化疗前、化疗后的外周血中CD4＋CD25＋调节性T细胞的分布特点。结果：（1）病例组化疗前外周血中CD4＋细胞比例显著低于对照组（P〈0．05）,CD4＋CD25＋调节性T细胞比例显著高于对照组（P〈0．05）;（2）病例组化疗后,CD4＋细胞比例明显高于化疗前（P〈0．05）,CD4＋CD25＋调节性T细胞比例明显低于化疗前（P〈0．05）;（3）病例组化疗后CD4＋细胞比例与对照组无显著差异（P〉0．05）,而CD4＋CD25＋调节性T细胞比例显著高于对照组（P〈0．05）。结论：非霍奇金淋巴瘤患者外周血中CD4＋CD25＋调节性T细胞比例升高,存在机体免疫抑制,化疗可降低CD4＋CD25＋调节性T细胞比例。     

培美曲塞联合顺铂对老年Ⅲ~Ⅳ期非小细胞肺癌患者血清CEA，CYFRA21-1，p-ERK，VEGF 及AnnexinⅡ水平的影响

目的:探讨培美曲塞联合顺铂对老年Ⅲ~Ⅳ期非小细胞肺癌患者血清癌胚抗原(CEA),细胞角质素片段抗原21-1(CYFRA21-1),磷酸化细胞外信号调节激酶(p-ERK),血管内皮生长因子(VEGF)及膜联蛋白Ⅱ(AnnexinⅡ)水平的影响。方法:120例老年Ⅲ~Ⅳ期非小细胞肺癌患者按抽签法分为对照组(n=60)与观察组(n=60),对照组予以多西紫衫醇联合顺铂治疗,观察组予以培美曲塞联合顺铂治疗,比较两组CEA,CYFRA21-1,p-ERK,VEGF,AnnexinⅡ,基质金属蛋白酶-2(MMP-2)及转化生长因子β1(TGF-β1),NK细胞,CD3~+,CD4~+,临床疗效和不良反应。结果:治疗后,观察组CEA,CYFRA21-1,p-ERK,VEGF,AnnexinⅡ,MMP-2及TGF-β1低于对照组,差异有统计学意义(P0.05)。观察组NK细胞,CD3~+及CD4~+高于对照组(P0.05)。观察组临床疗效、不良反应均优于对照组(P0.05)。结论:培美曲塞联合顺铂化疗可降低老年Ⅲ~Ⅳ期非小细胞肺癌患者血清CEA,CYFRA21-1,p-ERK,VEGF及AnnexinⅡ水平,控制肿瘤进展,值得推广。     

78例肺癌脑转移患者临床分析

目的：探讨与肺癌脑转移预后相关的影响因素,为更好的治疗肺癌脑转移提供参考依据。方法：回顾性分析2002年~2009年唐都医院收治的78例肺癌脑转移的临床资料。结果：患者年龄、性别、病理类型、脑转移灶数目、颅外有无转移性病灶、患者的行为状态（PS评分）对患者生存期无显著影响（P〉0.05）。但放疗＋化疗治疗组疗效显著优于单纯放疗组及单纯化疗组（P〈0.05）,症状消失者（CR）或明显缓解者（PR）生存较无明显改善者（SD）或加重者（PD）生存期显著延长。结论：对肺癌脑转移患者应采取放疗联合化疗综合方案治疗,同时,应及时关注其症状缓解情况并指导治疗。     

化疗联合放疗治疗非小细胞肺癌疗效观察

目的:研究化疗联合放疗治疗非小细胞肺癌的临床疗效及毒副作用.方法:58例非小细胞肺癌患者随机分为观察组与对照组两组各29例,观察组患者采用化疗联合放疗治疗,对照组患者只采用化疗治疗.观察比较两组患者的临床疗效、1,2,3年生存率及毒副作用.结果:观察组患者的有效率(79.3％)明显高于对照组(41.4％),两组相比差异有统计学意义(P＜0.05).观察组患者1,2,3年生存率均高于对照组,两组相比差异有统计学意义(P＜0.05,P＜0.01).两组患者的Ⅱ-Ⅳ级白细胞减少率,Ⅲ-Ⅳ级血红蛋白减少率,Ⅲ-Ⅳ级消化系统反应无显著差别,两组相比差异均无统计学意义(P＞0.05).结论:相对于单纯化疗,化疗联合放疗治疗非小细胞肺癌临床效果更好,毒副作用并未加重,可以显著提高患者生存率,值得临床推广应用.     

TKI治疗晚期tPd,细胞肺癌患者免疫功能的变化及意义

目的：通过观察晚期非小细胞肺癌患者TKI治疗前后外周血IgG、[gM、IgA、C3、c4、C-反应蛋白及CD3＋、CD4＋、CD8＋、CD4＋／CD8＋细胞的表达变化,探讨TKI治疗对晚期非小细胞肺癌患者免疫功能的影响及意义。方法：检测TKI组30例非小细胞肺癌患者TKI治疗前、治疗一个月后外周血IgG、IgM、IgA、C3、C4、C-反应蛋白及CD3＋、CD4＋,CD8＋、CD4＋／CD8＋细胞表达水平,分析表达变化及与疗效的关系。30例非小细胞肺癌患者作为对照组。结果：治疗前,TKI组与对照组IgG、IgM、IgA、C3、C4、c＋反应蛋白水平基本正常,但CD4＋细胞数量减低、CD4＋／CD8＋比值较低、CD8＋细胞数量增高,两组相比IgG、IgM、IgA、C3、C4、C-反应蛋白、CD3＋、CD4＋．CD8＋、CD4＋／CD8‘差异均无统计学意义（P〉0．05）;TKI治疗一个月后,TKI组与对照组IgG、IgM、IgA、C3、C4、C-反应蛋白水平无明显变化,而CD4＋细胞数量增多、CD4＋／CD8＋较前增高,CD8＋细胞数量较前减低,两组相比CD3＋、IgG、IgM、IgA、C3、C4、c-反应蛋白差异无统计学意义（P〉0．05）,而CD4＋．CD4＋／CD8＋、CD8＋差异有统计学意义（P〈O．01）。结论：TKI治疗后,晚期非小细胞肺癌患者细胞免疫功能得到改善,体现在CD4＋,CD8＋细胞数量的变化上,且TKI治疗的疗效可通过比较外周血CD4＋、CD4＋／CD8＋、cD8＋细胞表达变化体现。     

参一胶囊对晚期NSCLC 维持治疗的临床研究

目的:探讨晚期非小细胞肺癌(NSCLC)患者化疗获益后采用参一胶囊维持治疗的临床疗效。方法:选择2010年11月到2014年11月在我院经一线化疗后疗效评价无病情进展的120例晚期NSCLC患者,随机分为对照组(n=60)和实验组(n=60)。对照组仅接受定期随访观察,实验组采用参一胶囊维持治疗,比较两组患者治疗后的临床疗效、治疗前后免疫功能、生活质量的变化及不良反应的发生情况。结果:实验组患者的疾病控制率(DCR)明显高于对照组(P0.05)。治疗后,两组患者各免疫功能检测指标均低于治疗前,且实验组明显大于对照组(P0.05)。治疗后,实验组KPS评分提高率明显高于对照组(P0.05)。整个维持治疗过程中无治疗相关性死亡。结论:晚期NSCLC患者在化疗后采用参一胶囊维持治疗,可显著提高患者免疫功能、改善生活质量,且安全性良好,疗效显著,值得在临床上推广应用。     

Antiangiogenic effect of low-dose cyclophosphamide combined with ginsenoside Rg3 on Lewis lung carcinoma

Angiogenesis is now known to play an important role in both growth and metastasis of lung cancer. The intense interest in angiogenesis has led to a re-examination of the activity of many established cytotoxic agents. Some results of recent experimental studies have suggested that frequent administration of certain cytotoxic agents at low doses increases the antiangiogenic activity of the drugs. In the present study, we investigated the efficacy of the combination of low-dose cyclophosphamide and ginsenoside Rg3 for the antiangiogenic effect on Lewis lung carcinoma. Our findings suggest that continuous low-dose regimen of CTX increases the efficacy of targeting the tumor microvasculature, which produces therapeutic activity with decreased toxicity. The effects of the low-dose schedule of CTX may be further enhanced by concurrent administration of angiogenic inhibitor ginsenoside Rg3. As an antiangiogenic method, this regimen has the advantage of a reduced susceptibility to drug resistance mechanisms and improved animal survival.     

Biotransformation of ginsenosides Re and Rg1 into ginsenosides Rg2 and Rh1 by recombinant β-glucosidase

Ginsenosides Re and Rg1 were transformed by recombinant β-glucosidase (Bgp1) to ginsenosides Rg2 and Rh1, respectively. The bgp1 gene consists of 2,496?bp encoding 831 amino acids which have homology to the glycosyl hydrolase families 3 protein domain. Using 0.1?mg enzyme ml(-1) in 20?mM sodium phosphate buffer at 37°C and pH 7.0, the glucose moiety attached to the C-20 position of ginsenosides Re and Rg1, was removed: 1?mg ginsenoside Re ml(-1) was transformed into 0.83?mg Rg2?ml(-1) (100% molar conversion) after 2.5?h and 1?mg ginsenoside Rg1?ml(-1) was transformed into 0.6?mg ginsenoside Rh1?ml(-1) (78% molar conversion) in 15?min. Using Bgp1 enzyme, almost all initial ginsenosides Re and Rg1 were converted completely to ginsenosides Rg2 and Rh1. This is the first report of the conversion of ginsenoside Re to ginsenoside Rg2 and ginsenoside Rg1 to ginsenoside Rh1 using the recombinant β-glucosidase.     

人参皂苷Rg1对脑缺血再灌注大鼠Caspase-3蛋白表达的影响

目的探讨人参皂苷Rg1对脑缺血再灌注大鼠脑组织半胱氨酸天冬氨酸酶3(Caspase-3)表达的影响。方法将大鼠随机分为假手术组、模型组、人参皂苷Rg110、20、40mg/kg组、尼莫地平组,每组10只。采用线栓法栓塞大脑中动脉2h制作大鼠脑缺血再灌注模型;观察再灌注22h后神经功能缺损评分;应用免疫组化、免疫印迹法检测大脑皮层缺血半暗带Caspase-3的表达。结果(1)假手术组、模型组、人参皂苷Rg110、20、40mg/kg组和尼莫地平组神经功能缺损评分分别为0、2.8±0.9、2.1±0.9、1.5±0.7、1.3±1.1、1.5±0.7,差异有统计学意义(P0.05)。人参皂苷Rg120、40mg/kg组与模型组比较,差异有统计学意义(P0.05);人参皂苷Rg110mg/kg组与尼莫地平组比较,差异有统计学意义(P0.05);人参皂苷Rg120、40mg/kg组与尼莫地平组比较,差异均无统计学意义(P0.05)。(2)免疫组化和免疫印迹结果显示各组大鼠皮层缺血半暗带均有Caspase-3的表达,其中假手术组仅有少量表达,模型组表达最多。与模型组比较,人参皂苷Rg1各剂量组及尼莫地平组Caspase-3表达量减少,差异有统计学意义(P0.05);与尼莫地平组比较,人参皂苷Rg110mg/kg组的Caspase-3表达量显著增高,40mg/kg组显著降低(P0.05),而20mg/kg组则差异无统计学意义(P0.05)。结论人参皂苷Rg1防治脑缺血再灌注的机制与抑制脑组织Caspase-3表达有关,且以高剂量效果较好。     

Effects of ginsenoside Rg2 on the 5-HT3A receptor-mediated ion current in Xenopus oocytes

Treatment with ginsenosides, major active ingredients of Panax ginseng, produces a variety of pharmacological or physiological responses with effects on the central and peripheral nervous systems. Recent reports showed that ginsenoside Rg2 inhibits nicotinic acetylcholine receptor-mediated Na+ influx and channel activity. In the present study, we investigated the effect of ginsenoside Rg2 on human 5-hydroxytryptamine3A (5-HT3A) receptor channel activity, which is also one of the ligand-gated ion channel families. The 5-HT3A receptor was expressed in Xenopus oocytes, and the current was measured using the two-electrode voltage clamp technique. The ginsenoside Rg2 itself had no effect on the oocytes that were injected with H2O as well as on the oocytes that were injected with the 5-HT3A receptor cRNA. In the oocytes that were injected with the 5-HT3A receptor cRNA, the pretreatment of ginsenoside Rg2 inhibited the 5-HT-induced inward peak current (I5-HT) The inhibitory effect of ginsenoside Rg2 on I5-HT was dose dependent and reversible. The half-inhibitory concentrations (IC50) of ginsenoside Rg2 was 22.3 +/- 4.6 microM. The inhibition of I5-HT by ginsenoside Rg2 was non-competitive and voltage-independent. These results indicate that ginsenoside Rg2 might regulate the 5-HT3A receptors that are expressed in Xenopus oocytes. Further, this regulation on the ligand-gated ion channel activity by ginsenosides might be one of the pharmacological actions of Panax ginseng.     

Ginsenoside Rg1 protects rat cardiomyocyte from hypoxia/reoxygenation oxidative injury via antioxidant and intracellular calcium homeostasis

Ginsenoside Rg1 is a major active ingredient of Panax notoginseng radix which has demonstrated a number of pharmacological actions including a cardioprotective effect in vivo. This study investigated the protective effect and mechanism of ginsenoside Rg1 in cardiomyocytes hypoxia/reoxygenation (H/R) model. Pretreatment with ginsenoside Rg1 (60–120 µM) reduced lactate dehydrogenase release and increased cell viability in a dose‐dependent manner. Fluorescence analysis demonstrated ginsenoside Rg1 reduced intracellular ROS and suppressed the intracellular [Ca²⁺] level. Cell lysate detected an increase of T‐SOD, CAT, and GSH levels. The myocardial protection of ginsenoside Rg1 during H/R is partially due to its antioxidative effect and intracellular calcium homeostasis. J. Cell. Biochem. 108: 117–124, 2009. © 2009 Wiley‐Liss, Inc.     

Lack of dendritic cell mobilization into the peripheral blood of cancer patients following standard- or high-dose chemotherapy plus granulocyte-colony stimulating factor

BACKGROUND: Dendritic cells (DC), the most specialized antigen-presenting cells, can be detected in the peripheral blood (PB) and divided into two subsets of populations, DC1 and DC2, endowed with different functions. The aim of this study was to evaluate the effect on DC release and on their subsets of three regimens utilized to mobilize CD34+ cells into the PB in cancer patients and in normal CD34+ cell donors. PATIENTS AND METHODS: The mobilizing sequences were: standard-dose epirubicin+taxol+granulocyte-colony-stimulating factor (G-CSF; 15 patients with advanced breast cancer), high-dose cyclophosphamide (CTX)+G-CSF (10 patients with breast cancer patients and 7 with non-Hodgkin's lymphoma, NHL), and G-CSF alone (5 normal donors of CD34+ cells for allogeneic transplantation). Comparative data were obtained from the steady-state PB of 20 healthy volunteers. For flow cytometric analysis, DC were gated as negative for specific lineage markers (CD3, CD11b, CD14, CD16, CD56, CD19, CD20, CD34) and positive for HLA-DR. The DC1 and DC2 subsets were defined as CD11c and CDw123 positive, respectively. RESULTS: The percentages of DC at baseline and the time of CD34+ cell peak were: 0.48 and 0.51 for standard-dose chemotherapy (CT); 0.55 and 0.63 for breast cancer after high-dose CTX+G-CSF; 0.53 and 0.71 for NHL after high-dose CTX+G-CSF; and 0.51 and 0.54 for normal donors of CD34+ cells after G-CSF alone (all p=n.s.).Mean DC1/DC2 ratios in each study group at the time of CD34+ cell peak were 0.10, 0.12, and 0.18, respectively. Finally, in the group of healthy volunteers, the percentage of circulating DC was 0.95 and the mean DC1/DC2 ratio was 1.28. CONCLUSION: To our knowledge, this is the first report that demonstrates that both standard-dose or high-dose CT, when utilized together with G-CSF, do not induce DC mobilization into the PB, whereas a reversed DC1/DC2 ratio is observed. Furthermore, a lack of significant DC mobilization after G-CSF alone was also seen, in contrast to what was previously observed by others. These data should be taken in account when evaluating clinical correlations between DC number and CPC engraftment in both the transplantation setting, when monitoring the effects on the immune system of combinations of new drugs and/or cytokines, and when high numbers of DC are required for both experimental and clinical applications.     

Proteomic analysis effects of ginsenoside Rg1 on human umbilical vein endothelial cells stimulated by tumor necrosis factor-alpha

Ginsenoside Rg1 (derived from ginseng root) has been found to have many vasoprotective activities. The present study was undertaken to examine effect of ginsenoside Rg1 on the secretion of nitric oxide (NO) in human umbilical vein endothelial cells (HUVECs) stimulated with or without tumor necrosis factor-alpha (TNF-alpha). We showed here that ginsenoside Rg1 can increase the basal and TNF-alpha-attenuated NO production in a dose-dependent manner. As little is known regarding the vascular molecular mechanism of ginsenoside Rg1 on HUVECs and proteomic technique has more advantages in molecular identification, we attempted to use proteomic analysis to explain vascular molecular mechanism of ginsenoside Rg1 on HUVECs. Proteomic analytical result showed that 21 protein spots were changed in TNF-alpha stimulated HUVECs, including 9 up-regulated spots, 11 down-regulated spots, and 1 spot detected in TNF-alpha stimulated group only. The expression level of proteins such as MEKK3, phosphoglycerate mutase was increased, and nitric-oxide synthase, mineralocorticoid receptor were decreased in TNF-alpha stimulated HUVECs, while ginsenoside Rg1 could prevent this change or reverse to some degree. This study suggested that NO production increased via ginsenoside Rg1 played an important role in the protective effect on TNF-alpha stimulated HUVECs and was helpful to deeply understand the active mechanism of ginsenoside Rg1 to HUVECs at the molecular level.     

Ginsenoside Rg1 attenuates concanavalin A-induced hepatitis in mice through inhibition of cytokine secretion and lymphocyte infiltration

The effect of ginsenoside Rg1 (Rg1) on hepatic damage caused by concanavalin A (Con A) has not been fully elucidated. This study was designed to evaluate the protective effect of Rg1 on Con A-induced hepatitis in mice and explore the potential mechanisms of this effect. C57BL/6 mice were divided randomly into the following four experimental groups: phosphate-buffered saline group, Rg1 group, Con A group, Con A + Rg1 group. Mice received Rg1 (20 mg/kg) 3 h before intravenous administration of Con A (15 mg/kg). Levels of alanine transaminase, aspartate transaminase and cytokine production were measured, the amount of phosphorylated IκBα and p65 were tested, the numbers of CD4⁺ and CD8⁺ T lymphocytes infiltrated in the blood, spleen and liver were calculated, intercellular adhesion molecule-1 (ICAM-1) and interferon-inducible chemokine-10 (CXCL-10) levels were measured and histological examination of the livers was conducted. Pretreatment with Rg1 markedly reduced the elevated levels of serum aminotransferase, ameliorated liver damage and suppressed proinflammatory cytokines secretion via inhibition NF-κB activity following Con A injection of mice. Furthermore, Rg1 administration reduced ICAM-1 and CXCL-10 mRNA expression in the liver as well as the number of CD4⁺ and CD8⁺ T lymphocytes infiltrating in the liver. Rg1 reduced the incidence of liver damage through inhibition of the proinflammatory response and suppressed the recruitment of CD4⁺ and CD8⁺ T lymphocytes to the liver. These data indicate that Rg1 represents a novel agent for the treatment of T lymphocyte-dependent liver injury.     

Protective Effects of Ginsenoside Rg1 Against Colistin Sulfate-Induced Neurotoxicity in PC12 Cells

The present study aimed to examine the protective effect of ginsenoside Rg1 against colistin-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. Ginsenoside Rg1 was shown to elevate cell viability, decrease levels of malondialdehyde and intracellular reactive oxygen species, enhance activity of superoxide dismutase and glutathione, and decrease the release of cytochrome-c, formation of DNA fragmentation in colistin-treated PC12 cells. Ginsenoside Rg1 also reversed the increased caspase-9 and -3 mRNA levels caused by colistin in PC12 cells. These results suggest that ginsenoside Rg1 exerts a neuroprotective effect on colistin-induced neurotoxicity in PC12 cells, at least in part, via the inhibition of oxidative stress, prevention of apoptosis mediated via mitochondria pathway. Co-administration of ginsenoside Rg1 highlights the potential to increase the therapeutic index of colistin.