The possible role of interleukin-33 as a new player in the pathogenesis of contrast-induced nephropathy in diabetic rats

Figures & data

Table 1. The serum and kidney levels of IL-33, IL-6, and IL-1β of groups.

Parameters	Healthy rats (n = 6) (Mean ± SE)	Diabetic rats (n = 6) (Mean ± SE)	Diabetic rats with CN (n = 6) (Mean ± SE)
Serum creatinine (mg/dL)	0.71 ± 0.01	2.74 ± 0.07¶	3.27 ± 0.11* &
Serum urea (mg/dL)	6.49 ± 0.12	25.08 ± 0.61¶	33.24 ± 0.85* &
Serum IL-33 (ng/dL)	53.56 ± 1.04	61.15 ± 1.28¶	82.93 ± 1.14* &
Serum IL-6 (ng/dL)	106 ± 11.3	149 ± 7.9¶	226 ± 7.5 * &
Serum IL-1β (ng/dL)	27.3 ± 0.5	32.6 ± 1.3¶	46.2 ± 1.1*
Kidney tissue IL-33 (ng/g tissue)	3664 ± 75	7152 ± 79¶	7955 ± 132* &
Kidney tissue IL-6 (ng/g tissue)	1466 ± 33	4426 ± 16¶	4572 ± 31* &
Kidney tissue IL-1β (ng/g tissue)	3499 ± 10	4430 ± 26¶	5324 ± 124* &

Notes: ¶Diabetic rats versus healthy rats, p < 0.05.

*Diabetic rats with CN versus healthy rats, p< 0.05.

&Diabetic rats with CN versus diabetic rats, p < 0.05.

Figure 1. Photomicrographs of rat kidney (H&E, 200×). (A) HRs with normal histological appearance, (B) DRs, and (C) DRs + CN. Degenerative changes in tubuli (*) and glomeruli (arrowhead).

Figure 2. Immunohistochemical staining of IL-33 in rat kidney (200×). (A) HRs showed no immunopositivity, (B) DRs showed moderate immunopositivity in tubular cells (arrowhead), and (C) DRs + CN showed severe immunopositivity in tubular cells for IL-33 (arrowhead).

Table 2. Immunohistochemical staining of markers of inflammation, apoptosis, and autophagy in groups.

	Healthy rats	Diabetic rats	Diabetic rats with contrast-induced nephrology
IL-1β	0	2&	2*
IL-33	0	2&	2*
Bax	1	2&	3*
Bcl 2	1	2&	2*
Cleaved caspase 3	0	1&	2*¶
Caspase 3	1	2&	3*
Caspase 8	0	2&	3*¶
Caspase 9	1	1	2*¶
LC-3B	0	1&	2*¶
Beclin1	1	1	3*¶
ATG5	0	2&	2*

Notes: ATG5: Autophagy-related protein 5, IL: Interleukin, KIM1: kidney injury molecule 1, LC-3B: Light chain-3B.

&p < 0.05 for diabetic rats versus healthy rats.

*p < 0.05 for diabetic rats with contrast-induced nephrology versus healthy rats.

¶p < 0.05 for diabetic rats with contrast-induced nephrology versus diabetic rats.

Figure 3. Immunohistochemical staining of cleaved caspase-3 in rat kidney (200×). (A) HRs showed no immunopositivity, (B) DRs showed moderate immunopositivity in tubular cells (arrowhead) and glomeruli (arrow), and (C) DRs + CN showed severe immunopositivity for cleaved caspase-3 in tubular cells (arrowhead) and glomeruli (arrow).

Figure 4. Immunohistochemical staining of caspase-8 in rat kidney (200×). (A) HRs showed no immunopositivity, (B) DRs showed moderate immunopositivity in tubular cells (arrowhead) and glomeruli (arrow), and (C) DRs + CN showed severe immunopositivity for caspase-8 in tubular cells (arrowhead) and glomeruli (arrow).

Figure 5. Immunohistochemical staining of caspase-9 in rat kidney (200×). (A) HRs showed slight immunopositivity in intertubular areas, (B) DRs showed moderate immunopositivity in tubular cells (arrowhead) and glomeruli (arrow), and (C) DRs + CN showed severe immunopositivity for caspase-9 in tubular cells (arrowhead) and glomeruli (arrow).

Figure 6. Immunohistochemical staining of LC3B in rat kidney (200×). (A) HRs showed no immunopositivity, (B) DRs showed moderate immunopositivity in intertubular areas (arrowhead) and glomeruli (arrow), and (C) DRs + CN showed severe immunopositivity for LC3B in intertubular areas (arrowhead) and glomeruli (arrow).

Figure 7. Immunohistochemical staining of Beclin-1 in rat kidney (200×). (A) HRs showed no immunopositivity, (B) DRs showed moderate immunopositivity in intertubular areas (arrowhead) and glomeruli (arrow), and (C) DRs + CN showed severe immunopositivity for Beclin-1 in intertubular areas (arrowhead) and glomeruli (arrow).

Figure 8. Schematic presentation of the relationship between IL-33, apoptosis, and autophagy in diabetic patients with contrast-induced nephropathy.