Oxidative stress is thought to play an important role in the pathogenesis of inflammation not only through direct injurious effects, but also by involvement in molecular mechanisms [
1]. Among the complicated factors involved in the process of inflammation, reactive oxygen species (ROS) and reactive nitrogen species (RNS), such as the hydroxyl radical (
•OH), superoxide anion (O
2-), hydrogen dioxide (H
2O
2), nitric oxide (NO) and peroxynitrite (ONOO
-), appear to be critical elements. There is a large amount of evidence showing that the production of reactive species such as O
2•-, H
2O
2, and
•OH occurs at the site of inflammation and contributes to tissue damage [
2,
3]. By using inhibitors of NOS, the severity of inflammation was reduced, which demonstrates the role of NO
• in the pathogenesis associated with various models of inflammation [
4‐
6]. In addition to NO
•, ONOO
- is also generated during inflammation damage [
3,
6]. The involvement of ONOO
- in these conditions is strongly manifested by direct measurements. There is immunocytochemical documentation (increased nitrotyrosine immunoreactivity in the inflamed tissues) of augmented ONOO
- production in many inflammation diseases, such as ileitis [
7], endotoxin-induced intestinal inflammation [
8] and arthritis[
9]. Furthermore, the ability of ONOO
- to cause severe colonic inflammation has also been documented [
10]. Whereas, detoxification system for
•OH and ONOO
- in vivo has not been found; therefore, scavenging of
•OH and ONOO
- turns out to be a vital antioxidant process[
11]. It has been reported recently that H
2 selectively reduced
•OH and ONOO
-[
12]. So, as a free radical scavenger, H
2 may have the effect of anti-inflammation. Recently, molecular hydrogen has been proved effective in curing concanavalin A-induced hepatitis[
13] and colon inflammation induced by dextran sodium sulfate[
14]. However, inhalation of hydrogen gas may not be convenient for therapeutic use. A brief report has suggested that consumption of water containing hydrogen at a saturated level (hydrogen saline) reduces oxidative stress in rats[
15]. Thus, we expect to examine the effects of hydrogen saline on inflammation models.
Macrophages are considered to be an essential participant in inflammation [
16]. When activated by endotoxin, macrophages produce inflammatory cytokines, which in turn activate other macrophages and other nearby cells to promote more inflammatory cytokines. Tumor necrosis factor-alpha, as one of these inflammatory cytokines, has a decisive function in the process of inflammation[
17], and could represent the severity of inflammation.
In this study, we expect to examine whether the hydrogen saline has the anti-inflammation effect on both animal and cellular inflammation models.