糖尿病骨质疏松骨代谢生化标记物检测与分析

目的 探讨糖尿病骨质疏松血成纤维生长因子-23(FGF-23)、骨钙素(OCN)、I型胶原C-末端肽(CTX)的代谢水平与骨质疏松的关系。方法 将小鼠随机分成对照组、STZ组和US组三组,分别检测血清、尿液和骨中骨代谢的生物标志物的不同变化。结果 熊果酸衍生物(ursolic acid derivatives,UAD)可明显提高糖尿病小鼠骨钙含量、骨密度,促进FGF-23和OCN表达升高,降低PTH和CTX表达。结论 熊果酸衍生物通过促进新骨形成、抑制破骨细胞的骨吸收功能来改善STZ诱导的骨质疏松。     

龙花胶囊干预环磷酰胺致SD大鼠血小板减少症的实验研究

目的观察龙花胶囊对环磷酰胺致SD大鼠血小板减少症的影响。方法将40只SD大鼠随机分为空白组、模型组、龙花胶囊干预组及巨和粒对照组,每组10只,除空白组外,其余各组腹腔注射环磷酰胺造模,造模成功后,龙花胶囊干预组给予龙花胶囊溶液460 mg/kg灌胃,每日1次;巨和粒对照组给予巨和粒13μg/（kg.d）皮下注射;空白组和模型组灌胃等容积的0.9%氯化钠注射液,每日1次。各组均连续14 d,比较各组给药前后血小板计数、骨髓巨核细胞计数和血清血小板生成素（TPO）、白细胞介素-3（IL-3）水平。结果龙花胶囊干预组、巨和粒对照组在血小板计数、骨髓巨核细胞计数、血清TPOI、L-3水平上与模型组比较差异均有统计学意义（P〈0.05）;龙花胶囊干预组与巨和粒对照组比较差异无统计学意义（P〉0.05）。结论龙花胶囊可改善血小板减少症SD大鼠的一般情况,具有升高血小板计数,促进模型SD大鼠骨髓巨核细胞增殖,提高血清TPOI、L-3水平等作用。     

荞麦花叶提取物对S180荷瘤小鼠化疗的减毒增效作用

目的研究荞麦花叶提取物(extraction of buckwheat flower and leaf,EBFL)对环磷酰胺(CTX)化疗S180荷瘤小鼠的减毒和增效作用。方法建立小鼠S180实体瘤模型;大、小剂量治疗组分别ig荞麦花叶提取物20,40 mg/kg,连续给药14 d,测定荷瘤小鼠的生存期和化疗药物CTX的毒副作用,以及荞麦花叶提取物对CTX的减毒和增效作用。同时检测荞麦花叶提取物对淋巴细胞增殖、IL-2水平等免疫系统功能的影响。结果 EBFL对肿瘤抑制作用不明显但可使荷瘤小鼠生存率明显增高。与CTX伍用可发挥协同作用,提高荷瘤小鼠生存质量,体质量、白细胞计数、免疫器官指数,与CTX阳性对照组比较均显示显著差异(P<0.05或P<0.01)。结论荞麦花叶提取物可提高机体免疫力,延长生存期,同时减轻CTX的毒性。     

Therapeutic approaches to myeloma bone disease: an evolving story

Bone disease is a major morbidity factor in patients with multiple myeloma and significantly affects their overall survival. A complex interplay between malignant plasma cells and other marrow cells results in the generation of a microenvironment capable of enhancing both tumor growth and bone destruction. Bisphosphonates have consistently reduced the incidence of skeletal-related events in patients with multiple myeloma and other osteotropic tumors as well. However, their use is burdened with side-effects, including the risks of osteonecrosis of the jaw and kidney failure, suggesting that they should be discontinued after prolonged administration. New molecular targets of cell cross-talk in myeloma bone marrow are therefore under intensive investigation and new drugs are being explored in preclinical and clinical studies of myeloma bone disease. Compounds targeting osteoclast activation pathways, such as receptor activator of nuclear factor-κB/receptor activator of nuclear factor-κB ligand/osteoprotegerin, B-cell activating factor, mitogen-activated protein kinase and macrophage inflammatory protein-1α/chemokine receptor for macrophage inflammatory protein-1α axes, or soluble agents that improve osteoblast differentiation by modulating specific inhibitors such as Dickkopf-1 and transforming growth factor-β, as well as novel approaches of cytotherapy represent a new generation of promising drugs for the treatment of myeloma bone disease.     

Cardiospermum halicacabum inhibits Cyclophosphamide Induced Immunosupression and Oxidative Stress in Mice and also Regulates iNOS and COX-2 Gene Expression in LPS Stimulated Macrophages

The effect of a methanolic extract of Cardiospermum halicacabum L was studied against cyclophosphamide(CTX)-induced toxicity in mice. Administration of CTX (25 mg/kg b.wt, i.p.) for 10 days produced significantmyelosuppression as evidenced by a decreased WBC count and bone marrow cellularity. Co-treatment withCardiospermum significantly increased the total WBC count, bone marrow cellularity and α-esterase positivecells, and the relative organ weights of spleen as well as thymus compared to the CTX alone treated group.Cardiospermum further reduced the enhanced levels of ALP, GPT, LPO, and proinflammatory cytokine TNF-α,and also significantly increased the glutathione (GSH) level in CTX treated animals. The lowered levels ofother cytokines like IFN-γ, IL-2, GM-CSF, after CTX treatment were also found to be increased by extractadministration. Histopathological analysis of small intestine also suggested reduction of CTX-induced intestinaldamage. Moreover the extract down-regulated the inducible nitric oxide synthase (iNOS) and cyclo-oxygenase-2(COX-2) mRNA expression in LPS stimulated macrophages. These studies indicate that C. halicacabum couldreduce cyclophosphamide induced oxidative stress and immunosupression through enhancing the antioxidantstatus and immunomodulation by stem cell proliferation.     

环磷酰胺联合卡介苗对Lewis肺癌小鼠CD4~+CD25~+Treg细胞及效应细胞功能的影响

目的探讨环磷酰胺(CTX)联合卡介苗(BCG)治疗对Lewis肺癌小鼠CD4+CD25+Treg细胞和效应细胞功能的影响及CD4+CD25+Treg细胞与肿瘤的相关性。方法将传代培养的Lewis肺癌细胞接种于C57BL/6小鼠右腋皮下,建立Lewis肺癌模型。采用CTX联合BCG治疗,观察各组动物的肿瘤体积、脾脏CD4+CD25+Treg细胞数量和Foxp3 mRNA表达水平、脾脏T淋巴细胞增殖和杀伤功能。结果CTX联合BCG治疗组肿瘤生长较肿瘤组缓慢;联合治疗组小鼠脾脏CD4+CD25+Treg细胞数量明显低于肿瘤组(P<0.05);联合治疗组小鼠脾脏Foxp3 mRNA表达水平明显低于肿瘤组(P<0.05);联合治疗组小鼠脾脏T淋巴细胞增殖功能明显高于肿瘤组(P<0.05);联合治疗组小鼠脾脏CTLs细胞的杀伤活性略高于肿瘤组(P>0.05)。结论CTX联合BCG治疗可明显降低CD4+CD25+Treg细胞数量和Foxp3 mRNA表达水平,并增强机体抗肿瘤免疫应答,使肿瘤生长延缓。     

阴沟肠杆菌6株中产超广谱β内酰胺酶的基因型

目的：研究阴沟肠杆菌6株的超广谱β内酰胺酶(ESBLs)的基因型。方法：分别使用对TEM型、SHV型和CTX-M型基因特异的引物,PCR扩增6株阴沟肠杆菌接合子Esbl基因,对PCR产物直接测序分析其基因型。结果：3株阴沟肠杆菌的接合子均含有CTX—M-3型酶,同时含有TEM型酶。另3株阴沟肠杆菌接合子均含有一种等电点为8．3未知的β内酰胺酶,同时含有一种pI为5．4或5．5未知的β内酰胺酶。结论：临床分离的阴沟肠杆菌可产CTX-M-3型酶,对头孢菌素类产生耐药性。     

人参多糖注射液对环磷酰胺增效减毒作用实验研究

目的：研究人参多糖注射液对肿瘤的抑制作用及其对免疫功能的影响,并探讨其对环磷酰胺（CTX）化疗的增效减毒作用。方法：以S180瘤株ICR小鼠作为病理模型,随机分为模型组、未造模组、CTX组、联合用药组。连续给药10天后,测定其抑瘤率、白细胞数、胸腺指数和脾指数。同时复制CTX 致免疫低下小鼠模型,考察人参多糖注射液对血清溶血素和单核细胞吞噬功能的影响。结果：人参多糖注射液和CTX 合用时,能显著提高抑瘤率;同时减轻CTX 的毒副作用;对CTX 致免疫低下功能有一定的改善功能。结论：人参多糖注射液对CTX 具有明显的增效减毒作用。     

抗ENO1抗体联合二甲双胍通过靶向肿瘤干细胞逆转人非小细胞肺癌A549细胞对西妥昔单抗的抵抗

目的:探究抗烯醇化酶1 (enolase 1,ENO1)抗体、二甲双胍(metformin,MET)通过靶向肿瘤干细胞对西妥昔单抗(cetuximab,CTX)耐药型非小细胞肺癌A549细胞增殖、迁移、侵袭和干性的影响及其可能的作用机制.方法:10 mmol/L MET联合40μg/ml抗ENO1抗体处理CTX(35 ...