Amelioration effects of Kaempferol on immune response following chronic intermittent cold-stress.

Cold-stress causes disturbance of the homeostatic regulation of animals, and gradually impairs the immune and antioxidant functions of animals. Therefore, increasing the effectiveness of the immune response and antioxidant function are the most attractive strategies against cold-stress. Kaempferol (KPF) exerts both an anti-inflammatory and antioxidant pharmacological effect. However, nor much is known of the effects of KPF on providing protection from cold-induced intestinal oxidative damage and improving immunity. This study investigated the effects of KPF on immune factors and intestinal antioxidation in the blood of cold-stressed mice. KPF was solubilized in diluted saline before administration. The mice were randomly divided into 4 groups: (1) control, (2) cold-stress, (3) KPF 25 mg/kg, and (4) cinnamon (CAM) 30 mg/kg groups. Groups (2)-(4) were exposed to cold stress once a day for 7 days. Cold-stress was achieved by exposing the mice to a temperature of -15 °C and 70 ±â€¯10% humidity for 60 min, once a day. The histopathological changes in the small intestine of the mice were analyzed. The T lymphocyte populations in blood were measured using flow cytometry. The level of SLC6a4, 5-HT3 and 5-HTT in small intestine tissue was assessed using RT-PCR analysis. Cow blood samples were obtained for the hematological analysis. Kaempferol (KPF) (25 mg/kg) regularized the intestinal antioxidant activity in the cold stress animals. KPF was able to significantly (P < .05) return intestinal SLC6a4, 5-HT3 and 5-HTT levels to normal after it had increased due to cold-stress. KPF treatment prevented the cold stress-induced decrease in blood CD4+T cells and decrease CD8+T cells levels in mice. Improved hematological profiles were additionally observed on treatment cows with KPF. KPF compared favorably with cinnamon in cold stress management, suggesting cold stress disturbs the anti-inflammatory effect of KPF. Thus, KPF contributes to suppress the activated pro-inflammatory cytokines, IL-9, IL-13, CD8+T and neurochemicals, and to increase anti-inflammatory cytokines and CD4+T levels.