Anti-oxidative effects of silkworm storage protein 1 in HeLa cell

Silkworm hemolymph contains unique proteins that exhibit anti-apoptotic activity in mammalian cells. Among them, 30 K protein, which is one of the major anti-apoptotic molecules in silkworm hemolymph, has been well investigated. However, little is known about the biological functions of storage protein 1 (SP1), another main protein in silkworm hemolymph. In this study, the anti-apoptotic and anti-oxidative activities of SP1 were analyzed. A stable cell line expressing SP1 was constructed, which showed strong anti-apoptotic effect induced by staurosporine treatment. In addition, the cell line exhibited resistance to oxidative stress caused by hydrogen peroxide. For practical applications of SP1, recombinant SP1 was produced in Escherichia coli, and the supplementation of recombinant SP1 into culture medium exhibited anti-apoptotic and anti-oxidative activities. In addition, SP1 was found to be a cell-penetrating protein and localized in the cytosol as well as on the plasma membrane. The findings showed that SP1 itself is not an anti-oxidant; rather, it mediates intracellular anti-oxidative activity. In conclusion, the cellular resistance of SP1 to apoptosis and oxidative stress will provide a new strategy that could be utilized in the bio-industry for the production of biologics as well as for the development of anti-aging cosmetics.     

Hypoxia-inducible factor 1α regulates branching morphogenesis during kidney development

The kidneys are exposed to hypoxic conditions during development. Hypoxia-inducible factor (HIF), an important mediator of the response to hypoxia, is believed to have an important role in development. However, the relationship between HIF and branching morphogenesis has not been elucidated clearly.     

原发性高血压相关基因DNA甲基化的研究进展

高血压是常见的慢性疾病,也是心脑血管病最主要的风险因素。原发性高血压是由多基因和环境因素共同作用引起的复杂疾病,但具体的发病机制仍不清楚。随着研究的深入,DNA甲基化等表观遗传学因素在原发性高血压病理过程中起到的作用逐渐受到重视。本文总结了部分原发性高血压关联基因中DNA甲基化在其患病中的研究进展,阐述可受环境因素影响的DNA甲基标记与原发性高血压的关系,进一步了解高血压的发病机制。     

siRNA沉默整合素beta1 基因对子宫内膜癌细胞侵袭、转移的影响

目的：探讨siRNA 沉默整合素茁1 基因对子宫内膜癌细胞侵袭、转移的影响。方法：选取子宫内膜癌ECC-1细胞系(ER阳性) 和KLE细胞系(ER阴性)，分别转染Integrin beta1 siRNA 质粒(Integrin beta1 siRNA 组)、无义序列siRNA质粒(无义序列对照组)和空载 质粒(空载对照组)，利用实时荧光定量PCR 检测各组细胞中Integrin 茁1 mRNA的表达，Western blot 检测各组细胞中Integrin beta1、 beta-catenin 和C-Myc 蛋白的表达，Transwell 小室检测各组细胞迁移和侵袭能力，MTT 法检测各组细胞的增殖情况。结果：Integrin beta1 siRNA 组ECC-1 细胞和KLE 细胞中Integrin beta1 mRNA 和蛋白相对表达量均低于无义序列对照组和空载对照组(P<0.05)； Integrin beta 1 siRNA组ECC-1 细胞和KLE细胞中beta-catenin 蛋白和C-Myc 蛋白相对表达量均低于无义序列对照组和空载对照组， 差异均有统计学意义(P<0.05)；Integrin beta1 siRNA组ECC-1 细胞和KLE 细胞中迁移细胞数和侵袭细胞数均低于无义序列对照组 和空载对照组(P<0.05)；Integrin beta1 siRNA 组ECC-1细胞和KLE 细胞的A 值均低于无义序列对照组和空载对照组(P<0.05)。结 论：特异性抑制Integrin beta1 基因可抑制子宫内膜癌细胞迁移、侵袭和增殖，可能与抑制Wnt信号传导有关。     

Nesfatin-1 对营养性肥胖大鼠摄食量体重和胃排空率的影响

目的：通过颈静脉注射外源性nesfatin-1，观察营养性肥胖大鼠摄食、体重、胃排空率的变化情况。方法：营养性肥胖大鼠造模 成功后，各组大鼠行颈静脉插管手术，术后所有大鼠分为四组，正常对照组及肥胖对照组大鼠注射0.9%生理盐水，正常给药及肥 胖给药组大鼠注射外源性nesfatin-1（100 滋g·kg-1），连续颈静脉给药7 d，期间记录各组大鼠摄食量以及体重，给药结束后采用灌 胃酚红法测定大鼠胃排空率。结果：用高脂饲料连续饲养大鼠7天，正常对照组和正常nesfatin-1组大鼠的Lee’s指数分别为314.22 和314.44，肥胖对照组和肥胖nesfatin-1 组大鼠的Lee’s指数分别为318.22 和319.03，肥胖差异显著(T-test, P<0.01)，造模成功。连 续给药7 d 后，给药组摄食量和体重与对照组相比明显降低，但肥胖给药组摄食量及体重下降较正常给药组更加明显。胃排空率 与胃排出酚红量是成负相关的，实验中正常对照组和正常给药组的胃排空率分别是64.71± 4.51 和46.47± 3.20，而肥胖对照组和 肥胖给药组大鼠的胃排空率分别是75.67± 2.47 和50.88± 3.07，因此高剂量给予nesfatin-1 能显著降低大鼠的胃排空率。结论：综 上所述，长期持续外周静脉给予外源性的nesfatin-1 可以明显抑制正常及肥胖大鼠的摄食，动物体重减轻。