Human C-reactive protein accentuates macrophage activity in biobreeding diabetic rats.
Human C-reactive protein accentuates macrophage activity in biobreeding diabetic rats.
复制标题
DOI：
10.1016/j.jdiacomp.2012.03.020
复制
发表时间：
2013-01
影响因子：
3
通讯作者：
Devaraj S
中科院分区：
文献类型：
--
作者：
Jialal I;Kaur H;Devaraj S
1型糖尿病（T1DM）是一种促炎状态，其特征在于高C反应蛋白（CRP）水平。然而，缺乏研究CRP在促进糖尿病促炎状态中的作用的数据。因此，我们使用自发性糖尿病生物繁殖（BB）大鼠研究了人CRP的促炎作用。糖尿病大鼠（n = 9/组）连续3天注射人血清白蛋白（huSA）或人CRP（hCRP，20 mg/kg体重; i. p）。安乐死后获得血液和腹腔巨噬细胞（MPEG4）。采用腹腔巨噬细胞检测超氧阴离子释放、NF-κ B DNA结合活性、促炎介质分泌。与huSA相比，hCRP给药导致糖尿病大鼠中超氧阴离子产生显著增加，沿着细胞因子/趋化因子释放增加，以及纤溶酶原激活物抑制剂（PAI-1）和组织因子（TF）活性增加。与huSA相比，hCRP处理的BB大鼠MMPs显示出蛋白激酶C（PKC）-α、PKC-δ和p47 phox表达以及NF-κ B的显著诱导。因此，我们的数据表明，人CRP主要通过增加巨噬细胞活性在体内加剧糖尿病的促炎、促氧化和促凝血状态，这可能对血管并发症和抗炎治疗有影响。
Type 1 diabetes (T1DM) is a pro-inflammatory state characterized by high C-reactive protein (CRP) levels. However, there is a paucity of data examining the role of CRP in promoting the pro-inflammatory state of diabetes. Thus, we examined the pro-inflammatory effects of human CRP using spontaneously diabetic bio-breeding (BB) rats. Diabetic rats (n=9/group) were injected with Human serum albumin (huSA) or Human CRP (hCRP, 20 mg/kg body weight; i.p) for 3 consecutive days. Blood and peritoneal macrophages (MØ) were obtained following euthanasia. Peritoneal macrophages were used for measuring superoxide anion release, NF-κB DNA binding activity, proinflammatory mediator secretion. hCRP administration resulted in significantly increased superoxide anion production, along with increased release of cytokines/chemokines, and plasminogen activator inhibitor (PAI-1) and Tissue Factor (TF) activity in diabetic rats compared to huSA. hCRP-treated BB rat MØ showed significant induction of protein kinase C (PKC)-alpha, PKC-delta and p47 phox expression and NF-κB compared to huSA. Thus, our data suggests that human CRP exacerbates in-vivo the pro-inflammatory, pro-oxidant and procoagulant states of diabetes predominantly via increased macrophage activity and this could have implications with respect to vascular complications and anti-inflammatory therapies.
登录
查看更多内容
影响因子：
5.9
作者：
Bisoendial, Radjesh J.;Birjmohun, Rakesh S.;Stroes, Erik S. G.
通讯作者：
Stroes, Erik S. G.
影响因子：
8.2
作者：
Hansen, T. K.;Forsblom, C.;Groop, P. -H.
通讯作者：
Groop, P. -H.
DOI：
10.1084/jem.190.12.1733
发表时间：
1999-12-20
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Griselli M;Herbert J;Hutchinson WL;Taylor KM;Sohail M;Krausz T;Pepys MB
通讯作者：
Pepys MB
影响因子：
5.3
作者：
Hein, Travis W.;Singh, Uma;Vasquez-Vivar, Jeannette;Devaraj, Sridevi;Kuo, Lih;Jialal, Ishwarlal
通讯作者：
Jialal, Ishwarlal
影响因子：
7.7
作者：
Devaraj, S;Venugopal, SK;Jialal, I
通讯作者：
Jialal, I