Impact of endogenous hydrogen sulfide on toll-like receptor pathway in renal ischemia/reperfusion injury in rats

Figures & data

Figure 1. Expression of toll-like receptors in kidney after IRI. (A) Western blot analysis of TLR-2 and −4 in kidney after IRI. β-Actin served as internal control for semiquantification of TLR-2 and −4. Relative protein levels of TLR-2 (B) and TLR-4 (C) were compared among different groups. Notes: Data shown are mean ± SEM; *statistically significant from sham group (p < 0.05); γstatistically significant from IR group (p < 0.01); n = 3 each.

Figure 2. Increase of nuclear NF-κB p65, phosphorylated ASK1 and phosphorylated TRAF2 in kidney after IRI. (A) Western blot analysis of NF-κB p65, phosphorylated-ASK1 and TRAF2 in kidney after IRI. β-Actin served as internal control for semi-quantification of NF-κB p65, phosphorylated-ASK1 and TRAF2. Relative protein levels of NF-κB p65 (B), phosphorylated-TRAF2 (C) and ASK1 (D) were compared among different groups. Notes: Data shown are mean ± SEM; *statistically significant from sham group (p < 0.05); γstatistically significant from IR group (p < 0.01); n = 3 each.

Table 1. Histological evaluation of kidney sections for each group.

Animal groups	Histological scores	Morphology
Sham (n = 6)	1	Normal histological characteristics of glomeruli and tubules
IR (n = 6)	2.5*	Tubular cell degeneration, necrosis, cell swelling, brush border loss, tube formation and inflammatory cell infiltration
IR + PAG (n = 6)	4†	Tubular cell degeneration, necrosis, cell swelling, brush border loss, tube formation
IR + HA (n = 6)	4†	Tubular cell degeneration, necrosis, cell swelling, brush border loss, tube formation

Notes: Median of histological scores is shown.

IR, ischemia/reperfusion; PAG, propargylglycine; HA, hydroxylamine.

*Significantly different from sham group (p < 0.05).

†Significantly different from renal IR group (p < 0.05).

Figure 3. Histological evaluation of kidneys after IRI. (A) Representative histological photographs of kidney tissues from different groups. (B) Detailed histological scores of each group. Notes: Data shown are individual values and medians; *statistically significant from sham group (p < 0.05); γstatistically significant from IR group (p < 0.05); n = 6 each.

Figure 4. Expression of pro-inflammatory cytokines in kidney after IRI. Immunohistochemical analysis of IL-1β (A), IL-6 (B), IL-18 (C) and TNF-α (D) in kidney after IRI. Levels of IL-1β (E), IL-6 (F), IL-18 (G) and TNF (H) were compared among different groups. Notes: Data shown are mean ± SEM; *statistically significant from sham group (p < 0.01); γstatistically significant from IR group (p < 0.01); n = 6 each.

Figure 5. Apoptosis in kidney after IRI. (A) Representative photographs of TUNEL-stained kidney tissues from different groups. (B) Numbers of apoptotic cells were estimated and compared among different groups. Notes: Data shown are mean ± SEM; *statistically significant from sham group (p < 0.01); γstatistically significant from IR group (p < 0.05); n = 6 each.