Fig 1.
NO concentration and iNOS expression in RGK36 cells.
Intracellular NO concentration increased with L-arginine (A) while decreased with L-NIL (B). Data are expressed as the mean ± SD (n = 4). *p < 0.05, **p < 0.01. iNOS expression decreased with L-NIL (C, D). Data are expressed as the mean ± SD (n = 3). *p < 0.05.
Fig 2.
Expression of HCP-1 and HIF-1α in RGK36 cells. HCP-1, HIF-1α, and β-actin were detected by western blot.
Both HCP-1 and HIF-1α expression was increased with L-arginine (A-C), while it decreased with L-NIL (D-F) or 2-Me (G-I). Data are expressed as the mean ± SD (n = 3). *p < 0.05, **p < 0.01.
Fig 3.
Intracellular HpD accumulation in RGK36 and MKN45 cells.
Cells were treated with 10 mM L-arginine (A, D), 3 μM L-NIL (B, E), or 1 μM 2-Me (C, F) for 24 h. Then, the cells were exposed to culture medium containing 20 μM HpD for 6 h. Data are expressed as the mean ± SD (n = 4). *p < 0.05, **p < 0.01.
Fig 4.
The PDT effect was examined after exposure to HpD in RGK36 and MKN45 cells.
Cells were treated with 10 mM L-arginine (A, D), 3 μM L-NIL (B, E), or 1 μM 2-Me (C, F) for 24 h. Cell viability was evaluated after HpD exposure and laser irradiation. Data are expressed as the mean ± SD (n = 4). *p < 0.05, **p < 0.01.
Fig 5.
The activity of L-arginine was inhibited by 2-Me.
Expression of HCP-1 and HIF-1α in RGK36 cells was inhibited by 1 μM 2-Me (A-B). Data are expressed as the mean ± SD (n = 3). Intracellular HpD accumulation was also suppressed by 1 μM 2-Me (D). Data are expressed as the mean ± SD (n = 4). *p < 0.05 and **p < 0.01 vs control. ##p < 0.01 vs L-arginine. $p < 0.05 vs 2-Me.
Fig 6.
The mechanism of regulation of HCP-1 expression.
HCP-1 expression increase by L-arginine, while it decrease by L-NIL or 2-Me.