Table 2.

Minocycline regulates the gene expression of various pro-inflammatory and anti-inflammatory cytokines in brain homogenates after SAH

Gene name	SAH + vehicle	SAH + minocycline
macrosialin	2.44 ± 0.1****	1.06 ± 0.2####
IL-1β	1.63 ± 0.3***	0.87 ± 0.4####
TNF-α	2.51 ± 1.0***	0.91 ± 0.3####
TNFR1	0.97 ± 0.2 (ns)	0.81 ± 0.1 (ns)
TNFR2	1.24 ± 0.6 (ns)	0.9 ± 0.2 (ns)
IL-6	2.54 ± 0.6****	0.76 ± 0.5####
gp130	0.96 ± 0.2 (ns)	0.94 ± 0.3 (ns)
IL-6R	1.13 ± 0.4 (ns)	1.29 ± 0.3 (ns)
MMP9	1.54 ± 0.24****	1.05 ± 0.1####
TIMP1	0.23 ± 0.1**	3.13 ± 2.8###
COX2	2.09 ± 1.04****	0.74 ± 0.2###
iNOS	3.98 ± 1.27****	0.78 ± 0.5###
IL-10	0.38 ± 0.16****	1.57 ± 0.62####

Statistical significance was evaluated using one-way analysis of variance (Holm–Sidak method) indicating **^/## P < 0.01, ***^/### P < 0.001, and ****^/#### P < 0.0001 versus sham + vehicle (calculated as 1 for each target gene) and SAH + vehicle, respectively. Values are means ± standard error of mean (n = 3 animals per group). Each quantitative real-time polymerase chain reaction (qPCR) reaction was performed in triplicates. Each qPCR experiment was repeated twice. Gene expression for each gene was normalized to the expression of the housekeeping gene, glyceraldehyde-phosphate-dehydrogenase (GAPDH). The relative expression intensity was estimated by calculating 2^−ΔΔCt for each sample. For the calculation of the values displayed in the table, the control (sham + vehicle) was set as 1. The specificity of all polymerase chain reaction products was checked by a melting curve analysis

IL, interleukin, TNF-α, tumor necrosis factor α, TNFR, tumor necrosis factor receptor, gp130, glycoprotein 130, IL-6R, interleukin-6 receptor, MMP9, matrix metalloproteinase 9, ns, not significant, TIMP1, tissue inhibitor of MMP 1, COX2, cyclooxygenase 2, iNOS, inducible nitric oxide synthase

^*Significance with respect to sham

^#Significance with respect to the SAH + vehicle