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Table 2 mRNA expression of apoptotic, inflammatory, oxidative, antioxidant, and anti-inflammatory mediators in renal parenchyma after injury

From: Cyclosporine-assisted adipose-derived mesenchymal stem cell therapy to mitigate acute kidney ischemia–reperfusion injury

Variable Group 1 Group 2 Group 3 Group 4 Group 5 P value
Caspase 3 1* 1.24 ± 0.15 0.91 ± 0.09 0.88 ± 0.07 0.6 ± 0.06§ <0.0001
Bcl-2 1* 0.60 ± 0.06 0.73 ± 0.06 0.77 ± 0.06 0.94 ± 0.09§ <0.0009
TNF-α 1* 1.21 ± 0.09 0.88 ± 0.07 0.84 ± 0.04 0.56 ± 0.07§ <0.0001
MMP-9 1* 1.32 ± 0.1 0.94 ± 0.08 0.92 ± 0.04 0.69 ±0.05§ <0.0001
RANTES 1* 1.30 ± 0.04 1.03 ± 0.04 1.08 ± 0.06 0.84 ± 0.07§ <0.003
NOX-1 1* 1.30 ± 0.09 1.07 ± 0.05 1.03 ± 0.04 0.89 ± 0.05§ <0.007
HO-1 1* 1.43 ± 0.10 1.66 ± 0.09 1.92 ± 0.11§ 2.32 ± 0.11 <0.0001
NQO 1 1* 1.1 ± 0.07 1.22 ± 0.09 1.32 ± 0.04§ 1.44 ± 0.10 <0.0001
IL-10 1* 1.66 ± 0.07 1.60 ± 0.11 2.09 ± 0.06§ 2.75 ± 0.11 <0.0001
PGE-2 1* 0.82 ± 0.10 1.05 ± 0.07 1.17 ± 0.05§ 1.29 ± 0.07 <0.0001
eNOS 1* 0.62 ± 0.04 0.75 ± 0.05 0.89 ± 0.05§ 1.11 ± 0.04* <0.0001
  1. Relative changes in mRNA expression of apoptotic, inflammatory, oxidative, antioxidant, and anti-inflammatory mediators in renal parenchyma after ischemia–reperfusion injury (n = 8 in each group). Data expressed as mean ± standard deviation. eNOS, endothelial nitric oxide synthase; HO-1, heme oxygenase 1; MMP, matrix metalloproteinase; NOX, NAD(P)H oxidase; NQO, NAD(P)H quinone oxidoreductase; PGE2, prostaglandin E2; RANTES, regulated and normal T-cell expressed and presumably secreted. Group 1 = sham control; group 2 = ischemia–reperfusion (IR); group 3 = IR + cyclosporine (CsA); group 4 = IR + adipose-derived mesenchymal stem cells (ADMSC); group 5 = IR + CsA + ADMSC. Statistical analysis in each group by analysis of variance followed by Bonferroni multiple comparison post-hoc test. Symbols (*, †, ‡, §, ¶) indicate significance (at 0.05 level) by Bonferroni multiple-comparison post-hoc test: † vs. ‡ vs. § vs. ¶, all P <0.05 for inter-group comparisons.