Figure 10.

CXCR2 knockdown inhibits cisplatin-mediated expression of inflammatory genes response in rat cochlea. Male Wistar rats were injected with scramble or CXCR2 siRNA (siCXCR2 0.9 µg) by the trans-tympanic route, 48 h later animals followed by cisplatin (11mg/kg). Rats were sacrificed 72 h later, and their cochleae collected for RNA preparation. The expression levels of CXCR2, CXCR1, CXCL1, NOX3, iNOS, TNFα, IL-6, IL-10, STAT1, STAT3, COX2 genes are presented following normalization with GAPDH. Cisplatin induced inflammatory genes response, whereas knockdown of CXCR2 reduced cisplatin-induced response. The exception is STAT3 which was reduced by cisplatin and recovered in the CXCR2 knockdown group (P<0.0001 between vehicle cisplatin and siCXCR2+cisplatin, F(30,132)=28.97 and DF=132). (B) The ratio of STAT3:STAT1, derived from (A) was suppressed by cisplatin, normalized in the siCXCR2 + cisplatin group but significantly enhanced by siCXCR2. Data were presented as fold change mean ± SEM (n=4). Asterisks (*) indicate significant difference from vehicle group while (**) indicate significant difference form cisplatin group (n=4). Statistical analyses among groups were tested using one-way analysis of variance (ANOVA).