Curcumin alleviates spleen immunotoxicity induced by decabrominated diphenyl ethers (BDE-209) by improving immune function and inhibiting inflammation and apoptosis in broilers.

This study was conducted to assess the mitigating effects of curcumin (Cur) on immunotoxicity in the spleen of broilers induced by the polybrominated diphenyl ether BDE-209. Eighty one-day-old broilers were allocated to the following four groups: control group, BDE-209 (0.4 g/kg) group, BDE-209 (0.4 g/kg) + Cur (0.3 mg/kg) group, and Cur (0.3 mg/kg) group. Growth performance, immunological function, inflammation, and apoptosis were assessed after 42 days of treatment. The findings demonstrate that firstly, Cur restored spleen damage caused by BDE-209 by increasing body weight, decreasing feed-to-gain ratio, correcting the spleen index, and improving the histopathological structure of the spleen. Secondly, Cur relieved BDE-209-induced immunosuppression by increasing the levels of the immunoglobulins IgG, IgM, and IgA in the serum, as well as the levels of white blood cells and lymphocytes. The levels at which GATA binding protein 3, T-box expressed in T cells, interferon-γ, and interleukin (IL)- 4 are expressed were controlled. The ratio of T helper (Th) type 1 (Th1) to Th2 cells in the spleen of broilers was also controlled. Thirdly, Cur reduced the expression of Toll like receptor (TLR) 2, TLR4, nuclear factor (NF)-κB, IL-8, IL-6, and IL-1ß, which alleviated BDE-209-induced inflammation in broilers. Cur reduced BDE-209-induced apoptosis by increasing the expression of the bcl-2 protein, decreasing the expression of cleaved caspase-3 and bax proteins, decreasing the bax/bcl-2 protein ratio, and decreasing the mean optical density of TUNEL. These results suggest that Cur protects broiler spleens from BDE-209-induced immunotoxicity via modulating humoral immunity, the equilibrium between Th1 and Th2 cells, the TLRs/NF-κB inflammatory pathway, and the apoptotic pathway.

Dexmedetomidine attenuates hepatic ischemia-reperfusion injury-induced apoptosis via reducing oxidative stress and endoplasmic reticulum stress.

Dexmedetomidine (DEX) affords a hepatoprotective effect during ischemia-reperfusion (IR) injury (IRI); however, the underlying mechanism remains elusive. In this work, using a rat liver IR model and a BRL-3A cell hypoxia-reoxygenation (HR) model, we explored whether DEX protects the liver against IRI by decreasing oxidative stress (OS), endoplasmic reticulum stress (ERS), and apoptotic pathways. We found that DEX significantly increased SOD and GSH activity while decreasing ROS and MDA levels in BRL-3A cells, successfully preventing HR-induced OS damage. DEX administration reduced JNK, ERK, and P38 phosphorylation and blocked HR-induced MAPK signaling pathway activation. Additionally, DEX administration reduced the expression of GRP78, IRE1α, XBP1, TRAF2, and CHOP, which reduced HR-induced ERS. NAC prevented the MAPK pathway from being activated and inhibited the ERS pathway. Further research showed that DEX significantly reduced HR-induced apoptosis by suppressing the expression of Bax/Bcl-2 and cleaved caspase-3. Similarly, animal studies demonstrated DEX exerted a protective effect of the liver by alleviating histopathological injury and enhancing liver function, mechanically DEX reduced cell apoptosis in liver tissue by reducing oxidative stress and ERS. In conclusion, DEX mitigates OS and ERS during IR, thereby suppressing cell apoptosis, thus providing protection to the liver.