Involvement of prostaglandins and histamine in nickel wire-induced acute inflammation in mice

Involvement of prostaglandins and histamine in nickel wire-induced acute inflammation in mice
复制标题

DOI:
10.1002/jbm.a.32628
复制
发表时间:
2010-06-15
影响因子:
4.9
通讯作者:
Ohuchi, Kazuo
Ohuchi, Kazuo
中科院分区:
工程技术3区
文献类型:
--
作者:
Hirasawa, Noriyasu;Goi, Yoshiaki;Ohuchi, Kazuo

文献摘要

被引文献

相似文献

镍 (Ni) 离子的刺激性已在临床上得到充分证明。然而,参与固体镍引起的急性炎症的化学介质尚不完全清楚。我们在小鼠中使用镍丝植入模型,并检查了前列腺素和组胺在急性期血浆渗漏中的作用。将镍丝皮下植入小鼠背部 8 至 24 小时会引起血浆渗漏,并在 3 天时引起镍丝周围的组织坏死,而植入铝丝则不会引起此类炎症反应。植入后 4 小时,检测到镍丝周围细胞中环氧合酶 (COX)-2 和 HDC mRNA 的增加。吲哚美辛以剂量依赖性方式抑制8小时血浆渗漏。地塞米松和p38 MAP激酶抑制剂SB203580也抑制血浆渗出,这与抑制COX-2 mRNA的表达一致。此外,在组胺 H1 受体敲除小鼠和组氨酸脱羧酶 (HDC) 敲除小鼠中,血浆渗漏部分但显着减少,但在 H2 受体敲除小鼠中则没有。这些结果表明,从导线释放的Ni离子诱导COX-2和HDC的表达,导致炎症急性期血管通透性增加。 (C) 2009 Wiley periodicals, Inc. J Biomed Mater Res 93A: 1306-1311,2010
The irritancy of Nickel (Ni) ions has been well documented clinically. However, the chemical mediators involved in the acute inflammation induced by solid Ni are not fully understood. We used the Ni wire-implantation model in mice and examined roles of prostaglandins and histamine in plasma leakage in the acute phase. The subcutaneous implantation of a Ni wire into the back of mice induced plasma leakage from 8 to 24 h and tissue necrosis around the wire at 3 days, whereas the implantation of an aluminum wire induced no such inflammatory responses. An increase in the mRNA for cyclooxygenase (COX)-2 and HDC in cells around the Ni wire was detected 4 h after the implantation. The leakage of plasma at 8 h was inhibited by indomethacin in a dose-dependent manner. Dexamethasone and the p38 MAP kinase inhibitor SB203580 also inhibited the exudation of plasma consistent with the inhibition of the expression of COX-2 mRNA. Furthermore, plasma leakage was partially but siginificantly reduced in histamine H1 receptor knockout mice and histidine decarboxylase (HDC) knockout mice but not in H2 receptor knockout mice. These results suggested that the Ni ions released from the wire induced the expression of COX-2 and HDC, resulting in an increase in vascular permeability during the acute phase of inflammation. (C) 2009 Wiley Periodicals, Inc. J Biomed Mater Res 93A: 1306-1311,2010