| The study was conducted to investigate the effect of peroxisome proliferator-activated receptorγ(PPARγ) activation on immunological stress of piglets after lipopolysaccharide (LPS) challenge. Piglets were allotted to four treatments (6 replicates/treatment and 1 pig/replicate) including:①Control group (CONTR);②LPS challenged group (LPS);③LPS+ROS (PPARγagonist) (ROS);④LPS+ROS+bisphenol A diglycidyl ether (PPARγinhibitors) (BADGE). Blood samples were collected at 3h post-challenge. Following blood collection, the pigs were slaughtered to collect spleens, thymus, intestinal lymph nodes and livers for further analysis.In order to elucidate the regulatory effect of PPARγon immunological stress of piglets after LPS challenge, the experiment was conducted to investigate the effects of PPARγactivation on white blood cell differential count and blood biochemical analysis. The results showed that: (1) ROS alleviated the decrease of white blood cells and lymphocytes induced by LPS (P < 0.05). BADGE inhibited the effect of ROS on white blood cells; (2) ROS alleviated the increase of alkaline phosphatase (AKP) activity (P < 0.05) and the decrease of total protein, albumin and globulin (P < 0.1) induced by LPS. BADGE inhibited the effect of ROS (P < 0.1). These results indicate that ROS alleviates the change of white blood cell differential count and blood biochemical analysis induced by LPS, possible via PPARγ-dependent pathway.In order to study the regulatory effect of PPARγon oxidative stress of piglets after LPS challenge, the experiment was conducted to investigate the effects of PPARγactivation on oxidative and antioxidative indexes in plasma and tissues. The results showed that: ROS alleviated the decrease of superoxide dismutase (SOD) activity in spleens and livers (P < 0.05), and alleviated the increase of malonaldehyde (MDA) content in intestinal lymph nodes (P < 0.05) and myeloperoxidase (MPO) activity in thymus, livers (P < 0.05) and plasma (P < 0.1) induced by LPS. However, BADGE didn't affcet the role of ROS. These results indicate that ROS alleviates the oxidative stress induced by LPS, possible via PPARγ-independent pathway.In order to research the regulatory effect of PPARγon inflammatory response of piglets after LPS challenge, the experiment was conducted to investigate the effects of PPARγactivation on mRNA and protein expression of pro-inflammatory cytokines in plasma and tissues, and the hormone levels in plasma. The results showed that: (1) ROS did not alleviate the increase of mRNA of tumor necrosis factor-α(TNF-α) in spleens, intestinal lymph nodes (P < 0.05), thymus and livers (P < 0.1), and interleukin-6 (IL-6) in thymus (P < 0.05) induced by LPS. On the contrary, it aggravated the mRNA overexpression of pro-inflammatory cytokines. BADGE inhibited the effect of ROS on TNF-αmRNA in spleens, intestinal lymph nodes and livers (P < 0.05), and IL-6 mRNA in spleens (P < 0.05) and livers (P < 0.1). (2) ROS did not alleviate the increase of TNF-αand IL-6 protein in plasma and intestinal lymph nodes (P < 0.1), TNF-αprotein in spleens and IL-6 protein in livers (P < 0.05) induced by LPS. On the contrary, it aggravated the protein overexpression of pro-inflammatory cytokines. BADGE inhibited the effect of ROS on the expression of TNF-αand IL-6 protein in plasma, spleens and intestinal lymph nodes (P < 0.1). (3) ROS did not alleviate the increase of cortisol and prostaglandin E2 (PGE2) , and the decrease of insulin-like growth factor-1 (IGF-1) in plasma induced by LPS (P < 0.05). On the contrary, it aggravated the above-mention phenomena. BADGE inhibited the effect of ROS on cortisol (P < 0.1), PGE2 and IGF-1 (P < 0.05). These results indicate that PPARγactivation does not exert an anti-inflammatory effect, contrarily, it indeed exerts a pro- inflammatory effect.These results suggest that PPARγplays a bidirectional role on regulation of immunological stress of piglets induced by LPS. |
