Estrogen (E(2)) and progesterone (P) hormones have a pro-inflammatory and an anti-inflammatory role under different conditions. The current study explored this phenomenon in the context of septic inflammation.
Materials and methods: This study involved 48 female albino rats. E(2) (4 mg/100 g body weight (b.w.) and P (5 mg/kg b.w.) were administered to ovariectomized (OVX) rats after systemic inflammation (SI) induced by puncturing the caecum I cm from its end with a single hole by using a 21-gauge needle. Key indices of inflammation and apoptosis were evaluated.
Results: OVX animals subjected to SI showed significantly increased levels of serum tumor necrosis factor-alpha (TNF-u), C reactive protein (CRP) and alanine aminotransferase (ALT). They also showed higher levels of expression of the enzyme inducible nitric oxide synthase (iN OS); 312 ± 43 mg/ml; in the liver, and the activity of both cyclooxygenase 2 (COX-2); 59.4 ± 3.2 U/ml; and caspase 3 enzymes; 6.3 ± 0.54 ng/ml; when compared to non-OVX animals subjected to (SI), (180 ± 3 mg/ml, 16.4 ± 1.69 U/ml, 0.98 ± 0.23 ng/ml respectively). Administration of E(2) resulted in a significant reduction of all serum and liver tissue parameters of inflammation (e.g.decreased iNOS; 193 ± 28 mg/ml and COX-2; 27.6 ± 3.91 U/ml) and decreased apoptosis (Caspase 3; 1.18 ± 0.21 ng/ml). In contrast, OVX animals injected with P before induction of SI showed a significant rise of all measured parameters.
Conclusions: E(2) and Pin physiological levels have contrasting though complementary roles in regulation of the immune system possibly allowing a limited inflammatory response while preventing excessive damage to the tissues.
Keywords: apoptosis; liver; oestrogens; progesterone; systemic inflammation.