In addition, in CP-treated rats, PGE treatment induced the recovery of white blood cell, neutrophil, and lymphocyte counts, along with mid-range absolute counts, and increased the serum levels of inflammatory cytokines (TNF-α, IFN-γ, IL-2, and IL-12) and immunoglobulins (IgG and IgA).
Our results showed that incubation with CP significantly increases the percent of cell death, activities of caspase-3 and -9, level of TNF-α and also promotes the levels of biomarkers which play important role in oxidative stress.
Also, a significant increase in the risk of CP was observed to be associated with the interactions of TNF-αrs1799724 and MTHFR rs9651118 (OR 2.75, 95 % CI 1.23-6.13).
Statistically significant association was also found in patients with cPVL between TNFα TC, CC, GG, GG -1031/-857/-308/-238 genotypes combination (OR, 4.107; p=0.024), as well as IL1β TT, CC -511/+3954 genotypes combination (OR, 7.333; p=0.005) and risk of CP.
There is evidence that the amount of EPO in CP children is lower than in normal children, but the levels of proinflammatory cytokines, such as interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha, are higher in the CP children.
Factor 5, Factor 2, methylene tetrahydrofolate reductase, tumor necrosis factor-alpha, and other SNPs tested were not significantly associated with CP risk.