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1.
目的:趋化因子(CX3CL1)在神经性疼痛中起重要的生理病理作用,然而其在糖尿病神经病理痛中的作用还有待研究。本实验主要研究了在糖尿病小鼠痛阈下调的时间窗内,脊髓背角中趋化因子CX3CL1/趋化因子受体(CX3CR1)在触诱发痛发生与发展中的作用。创新点:主要探讨CX3CR1在链脲佐菌素(STZ)诱导的1型糖尿病(T1DM)小鼠早期发生的机械痛性神经病变中的作用。方法:本实验采用健康雄性C57BL/6小鼠与CX3CR1KO小鼠,体重20～23 g,隔夜禁食12 h(20点至次日8点),并连续三天腹腔注射100 mg/kg的STZ制备T1DM模型。以空腹血糖浓度11.1 mmol/L且三周后小鼠机械痛阈值明显下降的情况视为T1DM模型制备成功。在小鼠机械痛阈下降的对应时间点,取腰段脊髓背角,采用蛋白质印迹法(westernblot)和免疫组化法测定CX3CL1及CX3CR1的表达情况。同时,在发生机械痛阈值下降的第三周时间鞘内给予CX3CR1的中和抗体,进行机械刺激并观察其痛阈值的变化。结论:STZ诱导的T1DM动物模型在早期表现为显著的机械诱发痛,并伴随脊髓背角CX3CL1/CX3CR1表达上调;在痛阈下降期鞘内给予CX3CR1的中和抗体可抑制糖尿病小鼠的痛行为。与腹腔注射STZ形成T1DM的C57BL/6小鼠相比,CX3CR1基因敲除的糖尿病小鼠机械痛阈值下降的时间延迟,程度减轻。因此,我们推测CX3CL1/CX3CR1可能参与T1DM机械痛的形成与发展。  相似文献   

2.
目的:探讨嘌呤能离子通道型受体7(P2X7R)在链脲佐菌素(STZ)诱导的1型糖尿病(T1DM)小鼠早期发生的机械痛性神经病变中的作用。创新点:探讨脊髓P2X7R在T1DM产生痛性神经病变的早期阶段所起的作用,将有望为研究糖尿病痛性神经病变药物提供新的靶点。方法:本实验采用健康雄性C57BL小鼠与P2X7RKO小鼠(体重20～23克,从20点至次日8点隔夜禁食12小时)为研究对象,连续三天腹腔注射STZ(浓度为100 mg/kg),从而制备T1DM动物模型。如果空腹血糖11.1 mmol/L且三周后小鼠机械痛阈值明显下降,则表示模型制备成功。在小鼠机械痛阈下降的对应时间点,取腰段脊髓背角,采用蛋白质印迹法(western blot)和免疫组化方法测定P2X7R的表达情况。同时,在发生机械痛阈值下降的第3周时间鞘内给予其拮抗剂A740003,并进行机械刺激从而观察其痛阈值的变化。结论:STZ诱导的T1DM动物模型在早期表现为显著的机械诱发痛,并伴随脊髓背角P2X7R表达上调;在痛阈下降期鞘内给予其拮抗剂A740003可抑制糖尿病小鼠的痛行为。与腹腔注射STZ形成T1DM的C57BL/6小鼠相比,P2X7R基因敲除的糖尿病小鼠早期机械痛阈值下降的时间延迟,程度减轻。因此,我们推测P2X7R可能参与了STZ诱导的糖尿病小鼠早期机械痛性神经病变。  相似文献   

3.
目的:研究羌活与独活水煎液的抗炎及镇痛作用.方法:采用耳廓肿胀法观察羌活与独活水煎液的抗炎作用;采用福尔马林致痛模型观察羌活与独活水煎液的镇痛作用.结果:羌活水煎液明显减轻炎症肿胀度,抑制率为53％;羌活水煎液明显降低小鼠的疼痛分数(P＜0.05),独活水煎液降低小鼠的疼痛分数不明显(P＞0.05).结论:羌活水煎液具有显著的抗炎镇痛作用,独活水煎液抗炎镇痛效果不明显.  相似文献   

4.
目的:在失血性休克小鼠模型中使用不同的液体复苏,包括等渗盐水(NS)、高渗盐水(HTS)和羟乙基淀粉(HES),比较在不同时间点髓源性抑制细胞(MDSCs)在外周血、脾脏和骨髓组织中分布和分化的情况。创新点:(1)创建失血性休克小鼠模型;(2)将MDSCs引入失血性休克液体复苏后免疫变化的研究中;(3)对骨髓、脾脏和外周血细胞中的MDSCs分布进行研究,并探讨了在失血性休克不同液体复苏后MDSCs的分化趋势,为临床上形成规范的救治方案提供了科学的实践资料。方法:将BALB/c雄性小鼠随机分成四组,除对照组外,其余三组在建立失血性休克小鼠模型后采用不同的液体复苏:NS组、HTS组和HES组。在模型建立后的2、24和72 h分批次处死小鼠,取外周血、脾脏和骨髓细胞组织,通过三色荧光标记流式细胞术进一步分析MDSC细胞含量,以及其两亚组单核髓源性抑制细胞(M-MDSC)和中性粒髓源性抑制细胞(G-MDSC)的比值。结论:HTS可诱导MDSCs在外周血和脾脏中的早期积累,并影响MDSCs分化和分布;而HES对MDSCs的分布影响较小,但对MDSCs在骨髓中的分化影响较大。  相似文献   

5.
目的:通过对人参皂苷和三七皂苷多成分多水平均匀设计配伍的神经保护作用筛选研究,评价中药有效成分的均匀设计-高通量筛选技术。方法:选取人参皂苷Re,Rb1,Rg1,Rg3和三七皂苷R1等五种皂苷单体6个水平(1×10-4~1×10-9mol.L-1)进行均匀设计配伍组合,通过神经细胞血清剥夺损伤模型进行药效高通量筛选;得到的最佳组合样品,再通过小鼠脑缺血再灌注损伤模型(避暗法、断头耐缺氧实验)及血清和脑、心肌组织老化相关酶测定,进行药效学评价。结果:在细胞实验中筛选得到的最佳3个组合样品(A11,A12,P5),药效(细胞存活率>90%)高于1×10-4mol.L-1浓度的五种皂苷单体及维生素E(细胞存活率最高78%);可明显改善小鼠脑缺血再灌注损伤所致的记忆障碍,增强耐缺氧能力,提高组织超氧化物歧化酶(superoxide dismutase,SOD)活性,降低一氧化氮(nitric oxide,NO)含量,维持谷丙转氨酶(glutamic-pyruvic transaminase,ALT)及乳酸脱氢酶(lactic dehydrogenase,LDH)含量稳定(P<0.01~0.05)。结论:均匀设计配伍与...  相似文献   

6.
目的:探讨小鼠大脑皮层源性神经干细胞(NSCs)体外培养的两种方法并对培养的细胞进行鉴定.方法:分别取孕14～16d的昆明小鼠胚胎脑皮质并用细胞球悬浮培养和单层贴壁培养两种方法进行体外培养,用光学显微镜观察NSCs的生长情况,并用免疫细胞化学鉴定NSCs特异性抗原的表达,经过血清对NSCs分化诱导后进行胶质纤维酸性蛋白及微管相关蛋白-2的检测.结果:①培养出来的细胞可以扩增生长;②这两种方法分别培养的神经干细胞球和单层神经干细胞经抗巢蛋白免疫细胞染色均呈阳性;③两种培养方法培养出的NSCs经诱导分化后,免疫细胞化学染色显示微管相关蛋白-2、神经胶质酸性蛋白染色阳性.结论:采用无血清培养基中加入特定生长因子的神经干细胞球培养和单层贴壁两种培养技术,可培养出在体外稳定增殖并有多向分化潜能的NSCs.  相似文献   

7.
目的:观察实验性腹膜炎小鼠脾、肾钙调神经磷酸酶(CaN)在腹膜炎病程中变化。方法:36只小鼠随机分为6组,即腹膜炎48h、5d、10d、14d、21d组与对照组,腹膜炎组腹腔注射1%冰醋酸0.2mL,对照组腹腔注射等量生理盐水,每组各6只。采用比色法测定脾、肾组织CaN活性。结果:脾CaN活性在实验性腹膜炎5d、10d、14d、21d呈持续性低水平(P<0.01);肾CaN活性在实验性腹膜炎10d达高峰14d、21d与10d相比呈下降趋势但仍高于对照组,差异有显著性。结论:实验性腹膜炎小鼠脾、肾CaN活性变化与病程进展有关。  相似文献   

8.
目的:本文探析了小鼠在低氧环境下的耐受情况,以及低氧后小鼠海马中脑源性神经营养因子(Brain derived neurotrophic factor,BDNF)基因的表达变化,为后续低氧与低氧预适应对BDNF的机制研究提供了参考依据.方法 :在建立小鼠低氧模型后,通过PCR(Polymerase chain reaction)技术从基因水平快速、简便地扩增BDNF基因.结果:随着低氧次数的增加,小鼠的低氧耐受明显增加了,并且BDNF的基因表达也明显增加.  相似文献   

9.
桑寄生浸膏的抗炎和镇痛作用研究   总被引：2，自引：0，他引：2  
目的：研究中药桑寄生水提部位的抗炎和镇痛作用。方法：以生理盐水和阿司匹林为对照,采用小鼠热板法、扭体法、腹腔毛细血管通透法和耳肿胀法对不同剂量桑寄生浸膏的抗炎和镇痛作用进行考察。结果：桑寄生浸膏能显著延长小鼠的疼痛反应时间,明显减少小鼠的扭体次数;并能显著缓解乙酸所致小鼠腹腔毛细血管通透性的增高,减轻二甲苯所致小鼠的耳肿胀程度,并加速消退,抗炎和镇痛作用良好。结论：桑寄生浸膏具有显著的镇痛和抗炎作用,效果与阿司匹林相近,可作为祛风湿用药。  相似文献   

10.
目的:研究人参皂甙Rg1对小鼠脂肪干细胞神经样分化的促进作用,并初步探讨其作用机理。创新点:证明了人参皂甙Rg1可以通过mi RNA-124途径促进脂肪干细胞的神经样分化。方法:从BALB/c小鼠腹股沟和睾丸脂肪垫处分离培养脂肪干细胞,利用流式细胞仪检测分离的脂肪干细胞纯度。试验分为以下五组:磷酸缓冲盐溶液(PBS)组、3-异丁基-1-甲基黄嘌呤(IBMX)组、IBMX+Rg1低剂量组、IBMX+Rg1中剂量组和IBMX+Rg1高剂量组。用细胞免疫组化方法检测了脂肪干细胞向神经样细胞的分化效率,用荧光定量聚合酶链式反应(qP CR)方法检测mi RNA-124的表达变化,用免疫印迹的方法检测巢蛋白(nestin)、βIII-微管蛋白(βIII-tubulin)及羧基端小结构域磷酸酶1(SCP1)的表达水平。结论:免疫组化结果显示,IBMX可以成功诱导小鼠脂肪干细胞向神经样细胞的分化;免疫印迹结果显示,Rg1可以显著提高神经样细胞标记蛋白的表达水平;荧光定量PCR结果显示,Rg1可以促进miRNA-124的表达量,进而降解神经分化抑制因子SCP1的表达,促进脂肪干细胞的神经样分化效率。  相似文献   

11.
The objective was to investigate the expression of bone morphogenetic protein (BMP) family members in the mouse uterus during the estrous cycle by real-time polymerase chain reaction (PCR) and immunohistochemistry. Uterine samples from Swiss ICR mice were collected and dissected free of surrounding tissue. One uterine horn was snap frozen in liquid nitrogen immediately after collection and stored at −80 °C for RNA extraction, and the other was fixed in 40 mg/ml paraformaldehyde at room temperature for immunolocalization of BMP2 protein. Real-time PCR analysis showed that the expression level of Bmp2 was significantly higher at proestrus than at estrus and metestrus (P<0.05). The relative abundance of Bmp4 exhibited significant fluctuations, but there were no statistically significant differences between the expression levels of Bmp2 and Bmp4 (P>0.05). The expression levels of Bmpr1a and Bmpr2 remained unchanged during estrous cycles. However, the level of Bmpr1b mRNA decreased significantly at estrus (P<0.05), increasing subsequently at metestrus. Furthermore, the level of Bmpr1b mRNA was significantly lower than those of Bmpr1a and Bmpr2 mRNA at the corresponding stages (P<0.05). All three receptor-regulated Smads (R-Smads) detected were differentially expressed in the mouse uterus and the expression levels of Smad1 and Smad5 were significantly higher than that of Smad8 (P<0.05). In addition, the expression level of Smad4 did not change substantially throughout the estrous cycle. Immunohistochemical experiments revealed that BMP2 protein was differentially expressed and localized mainly in the uterine luminal and glandular epithelial cells throughout the estrous cycle. In conclusion, our results provide information about the variation in the mRNA levels of Bmp2 and Bmp4 and related components of the BMP signaling pathway. The data provide quantitative and useful information about the roles of endometrial BMP proposed and demonstrated by others, such as the degradation and remodeling of the endometrium.  相似文献   

12.
Objective: To investigate the protective effects and mechanisms of action of dexamethasone and Salvia miltiorrhiza on multiple organs in rats with severe acute pancreatitis (SAP). Methods: The rats were divided into sham-operated, model control, dexamethasone treated, and Salvia miltiorrhiza treated groups. At 3, 6, and 12 h after operation, the mortality rate of different groups, pathological changes, Bcl-2-associated X protein (Bax) and nuclear factor-κB (NF-κB) protein expression levels in multiple organs (the pancreas, liver, kidneys, and lungs), toll-like receptor 4 (TLR-4) protein levels (only in the liver), intercellular adhesion molecule 1 (ICAM-1) protein levels (only in the lung), and terminal deoxynucleotidy transferase mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) staining expression levels, as well as the serum contents of amylase, glutamate-pyruvate transaminase (GPT), glutamic-oxaloacetic transaminase (GOT), blood urea nitrogen (BUN), and creatinine (CREA) were observed. Results: The mortality rate of the dexamethasone treated group was significantly lower than that of the model control group (P<0.05). The pathological changes in multiple organs in the two treated groups were relieved to different degrees (P<0.05 and P<0.01, respectively), the expression levels of Bax and NF-κB proteins, and apoptotic indexes of multiple organs were reduced (P<0.05 and P<0.01, respectively). The contents of amylase, GPT, GOT, BUN, and CREA in the two treated groups were significantly lower than those in model control groups (P<0.05 and P<0.01, respectively). The expression level of ICAM-1 protein in the lungs (at 3 and 12 h) in the dexamethasone treated group was significantly lower than that in the Salvia miltiorrhiza treated group (P<0.05). The serum contents of CREA (at 12 h) and BUN (at 6 h) of the Salvia miltiorrhiza treated group were significantly lower than those in the dexamethasone treated group (P<0.05). Conclusions: Both dexamethasone and Salvia miltiorrhiza can reduce the inflammatory reaction, regulate apoptosis, and thus protect multiple organs of rats with SAP.  相似文献   

13.
To investigate the effects of hypoxic exercise training on microRNA (miRNA) expression and the role of miRNA expression in regulating lipid metabolism, 20 dietary-induced obese SD rats were divided into a normoxic sedentary group (N, n=10) and a hypoxic exercise training group (H, n=10). After four weeks, measurements were taken of body weight, body length, fat mass, serum lipid concentration, miRNAs differentially expressed in rat liver, and gene and protein expression levels of peroxisome proliferator activated receptor α (PPARα), fatty acid synthetase (FAS), and carnitine palmitoyl transferase 1A (CPT1A) in rat liver. Body weight, Lee’s index, fat mass, fat/weight ratio, and serum levels of total cholesterol (TC) and high density lipoprotein cholesterol (HDL-C) were all significantly lower in the H group than in the N group (P<0.01). Six miRNAs expressed significantly differently in the liver (P<0.05). Specifically, expression levels of miR-378b were significantly lower in the H group than in the N group (P<0.05). Compared with the normoxic sedentary group, hypoxic exercise training resulted in a lower ratio of FAS mRNA to CPT1A mRNA (P<0.05), as well as lower CPT1A protein levels (P<0.01), while a higher ratio of FAS to CPT1A protein levels (P<0.01) was observed. In conclusion, hypoxic training may elevate the resistance of high fat diet induced obesity in rats by reducing the expression of miR-378b, and decrease the fatty acid mitochondrial oxidation in obese rat livers by decreasing the protein expression of CPT1A and increasing the protein expression ratio of FAS/CPT1A.  相似文献   

14.
Background and objective: Non-alcoholic fatty liver disease (NAFLD) is associated with arterial stiffness in the general population. Age, obesity, hypertension, and diabetics are risk factors for arterial stiffness. In this study, we aimed to investigate the association between NAFLD and arterial stiffness as measured by brachial-ankle pulse wave velocity (baPWV) in the non-obese, non-hypertensive, and non-diabetic young and middle-aged Chinese population. Methods: A cross-sectional study with 1296 non-obese, non-hypertensive, and non-diabetic young and middle-aged (20–65 years) subjects undergoing routine medical check-ups in the International Health Care Center of the Second Affiliated Hospital of School of Medicine of Zhejiang University was carried out. Fatty liver was diagnosed by ultrasonography, and baPWV was measured using an automatic waveform analyzer. The subjects were classified into two groups according to the presence of NAFLD, and divided into a further two groups according to their baPWV. Results: The overall incidence of NAFLD was 19.0%, and NAFLD patients had a significantly higher level of baPWV than the controls ((1321±158) cm/s vs. (1244±154) cm/s; P<0.001). The incidence of NAFLD was clearly higher in the increased baPWV group than in the normal baPWV group (29.3% vs. 16.9%; P<0.001), and the incidence increased in line with the increase of baPWV quartiles in the normal range as well as with the severity of arterial stiffness (both P for trend <0.001). Multiple linear logistic regression analysis showed that the presence of NAFLD was positively and independently associated with baPWV. Conclusions: Our results suggest that the presence of NAFLD is associated with arterial stiffness as measured by baPWV in the non-obese, non-hypertensive, and non-diabetic young and middle-aged Chinese population.  相似文献   

15.
Background and objective: Gonadotropin-releasing hormone (GnRH) plays an important role in the regulation of ovarian function and ovarian cancer cell growth. In this study, we determined whether administration of the GnRH agonist (GnRHa), triporelin, prior to cisplatin treatment affects cisplatin and/or prevents cisplatin-induced ovarian damage. Methods: nu/nu mice were injected with ovarian cancer OVCAR-3 cells intraperitoneally. After two weeks, the mice were treated with saline (control), cisplatin, GnRHa, or cisplatin plus GnRHa for four weeks. At the end of the experimental protocol, blood, tumor, ovary, and uterine tissues were resected for hematoxylin and eosin (H&E) staining, immunohistochemical analyses of Ki67, nuclear factor-κB (NF-κB), and caspase-3, transmission electron microscopy of apoptosis, or enzyme-linked immunosorbent assay (ELISA) analyses of anti-Mullerian hormone (AMH). Results: Cisplatin treatment effectively inhibited tumor growth in mice treated with human ovarian cancer cells; however the treatment also induced considerable toxicity. Immunohistochemical analyses showed that Ki67 expression was reduced in cisplatin-treated mice compared to control (P<0.05), but there was no statistically significant differences between cisplatin-treated mice and cisplatin plus GnRHa-treated mice (P>0.05), while expressions of NF-κB and caspase-3 were reduced and induced, respectively, in cisplatin-treated mice and cisplatin plus GnRHa-treated mice. Apoptosis occurred in the GnRHa, cisplatin, and cisplatin plus GnRHa-treated mice, but not in control mice. Ovaries exposed to GnRHa in both GnRHa mice and cisplatin-treated mice (combination group) had significantly more primordial and growth follicles and serum levels of AMH than those in the control mice and cisplatin-treated mice (P<0.05). Conclusions: Administration of GnRHa to mice significantly decreased the extent of ovarian damage induced by cisplatin, but did not affect the anti-tumor activity of cisplatin.  相似文献   

16.
目的:探讨细胞色素P450 2D6*10(CYP2D6*10)基因遗传多态性,并评估其对他莫昔芬联合十一酸睾酮治疗特发性少精男性不育症患者血清性激素、精液参数及自然妊娠率的影响。方法:该病例对照研究包括230例特发性少精男性不育患者和147例正常对照。病例组服用枸橼酸他莫昔芬20 mg/d和十一酸睾酮40 mg/d,疗程共6个月。采用Hph I内切酶对CYP2D6*10基因聚合酶链式反应(PCR)产物进行内切后,从而对其分型。分别于研究开始时、3月及6月分别检测研究对象性激素水平、精液参数及配偶自然妊娠率。结论:CYP2D6*10基因突变型特发性少精男性不育患者接受他莫昔芬联合十一酸睾酮疗效较基因野生型组差。  相似文献   

17.
This study aims to elucidate the antiproliferative mechanism of hydroxychavicol(HC).Its effects on cell cycle,apoptosis,and the expression of c-Jun N-terminal kinase(JNK)and P38 mitogen-activated protein kinase(MAPK)in HT-29 colon cancer cells were investigated.HC was isolated from Piper betle leaf(PBL)and verified by high-performance liquid chromatography(HPLC),nuclear magnetic resonance(NMR),and gas chromatography-mass spectrometry(GC-MS).The cytotoxic effects of the standard drug 5-fluorouracil(5-FU),PBL water extract,and HC on HT-29 cells were measured after 24,48,and 72 h of treatment.Cell cycle and apoptosis modulation by 5-FU and HC treatments were investigated up to 30 h.Changes in phosphorylated JNK(pJNK)and P38(pP38)MAPK expression were observed up to 18 h.The half maximal inhibitory concentration(IC50)values of HC(30μg/mL)and PBL water extract(380μg/mL)were achieved at 24 h,whereas the IC50of 5-FU(50μmol/L)was obtained at 72 h.Cell cycle arrest at the G0/G1 phase in HC-treated cells was observed from12 h onwards.Higher apoptotic cell death in HC-treated cells compared to 5-FU-treated cells(P<0.05)was observed.High expression of pJNK and pP38 MAPK was observed at 12 h in HC-treated cells,but not in 5-FU-treated HT-29 cells(P<0.05).It is concluded that HC induces cell cycle arrest and apoptosis of HT-29 cells,with these actions possibly mediated by JNK and P38 MAPK.  相似文献   

18.
目的:研究离体热处理和顺铂联合热处理对术中回收血红细胞功能的影响及其中混杂的肝肿瘤细胞株(HepG2)的杀灭作用。创新点:(1)采用多种评价指标研究了不同时间离体热处理对术中回收血中混杂的HepG2的杀灭作用及对红细胞的影响,并确定了对红细胞安全且能有效杀灭HepG2的离体热处理时间。(2)从多个角度评价了离体顺铂联合热处理对术中回收血红细胞的影响及对其中混杂的HepG2的杀灭作用,确定了该方案中对红细胞安全且能有效去除HepG2的顺铂浓度。方法:采用3-(4,5-二甲基噻唑-2)-2,5-二苯基四氮唑溴盐(MTT)、5-乙炔基-2’脱氧尿嘧啶核苷(EdU)和平板克隆形成评估HepG2的细胞存活率、DNA复制率和克隆形成能力(图1和3);从红细胞渗透脆性、携氧能力(2,3-二磷酸甘油酸(2,3-DPG)、半饱和氧分压(P50))、能量代谢(Na+-K+-ATPase、pH)、膜完整性(游离血红蛋白(Hb)、血清K+和Na+浓度、细胞膜磷脂酰丝氨酸外翻比例)等角度评估红细胞功能(图2和4;表3)。结论:肝肿瘤术中回收血经离体顺铂联合热处理(42°C,50μg/ml)60min后,能有效清除其中混杂的HepG2,但对红细胞无显著影响,值得体内进一步研究顺铂热处理有效应用于肿瘤手术自体血液回输的安全方案。  相似文献   

19.
In the present study, we investigated the possible toxicity mechanism of lipopolysaccharide (LPS) extracted from Gram-negative bacteria in Eriocheir sinensis hemocytes. Apoptotic hemocytes and reactive oxygen species (ROS) production induced by the LPS were monitored by the combination of flow cytometry and microscope observation. It was shown that LPS induced serious damage on the DNA and morphological changes in hemocytes, including cell shrinkage, fracture of nucleus membrane, margination, condensation and fragmentation of chromatin, and formation of apoptotic bodies indicating obvious hemocyte apoptosis. As compared with the control group, the apoptotic cell ratio increased to 30.61% and 39.01% after 1-h exposure and 57.72% and 75.01% after 2-h exposure to 1 and 10 μg/ml LPS, respectively (P<0.05). Significant outburst of ROS production was observed in LPS-treated hemocytes with approximately 176.6% of relative dichlorofluorescein mean fluorescence at 1-h exposure, followed by a drastic decline (P<0.05). These results indicated that LPS would induce oxidative stress on hemocytes from E. sinensis and cause ROS burst, DNA damage, and subsequently apoptosis. The process of ROS-mediated apoptosis might be one of the potential toxicity mechanisms of LPS on crustacean hemocytes.  相似文献   

20.
Objective: XRCC1 polymorphism is a research hotpot in individual treatment for non-small cell lung cancer (NSCLC). To obtain the association between XRCC1 polymorphism and clinical outcome of platinum-based treatment for NSCLC, a meta-analysis was conducted. Methods: Databases including PubMed, Embase, Cochrane, and Chinese National Knowledge Infrastructure (CNKI) were searched for publications that met the inclusion criteria. A fixed effect model was used to estimate pooled odds ratio (OR) and hazard ratio (HR) with 95% confidence interval (CI) for the association between XRCC1 Arg399Gln and response or survival of platinum-based treatment for advanced NSCLC. A chi-squared-based Q-test was used to test the heterogeneity hypothesis. Egger’s test was used to check publication bias. Results: Seventeen published case-control studies that focus on the association between XRCC1 Arg399Gln and response or survival of platinum-based treatment for advanced NSCLC in 2 256 subjects were included in this meta-analysis, of whom 522 were AA genotypes (23.2% frequency), 916 AG genotypes (40.6% frequency), and 818 GG genotypes (36.2% frequency). The overall response rate (ORR) was 45.2% (110/243) for AA genotype patients, 29.9% for AG genotype (73/244), and 30.7% for GG genotype (124/403). The heterogeneity test did not show any heterogeneity and the Egger’s test did not reveal an obvious publication bias among the included studies. The meta-analysis indicated that AA genotype patients presented higher response rates toward platinum drug treatment compared with G model (GG+GA) patients (GG vs. AA model: OR=0.489, 95% CI 0.266–0.900, P=0.021; AG vs. AA model: OR=0.608, 95% CI 0.392–0.941, P=0.026; GA+AA vs. GG model: OR=1.259, 95% CI 0.931–1.701, P=0.135; GG+GA vs. AA model: OR=0.455, 95% CI 0.313–0.663, P=0.0001). However, no evidence validates XRCC1 associates with the survival following platinum drug therapy. Conclusions: Our meta-analysis suggested that XRCC1 Arg399Gln is related with the sensitivity of NSCLC patients to platinum-based treatment. AA genotype patients present more desirable curative effectiveness compared with other patients.  相似文献   

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