Nano-CaCO 3 /polypropylene (PP) composites modified with polypropylene grafted with acrylic acid (PP-g-AA) or acrylic acid with and without dicumyl peroxide (DCP) were prepared by a twin-screw extruder. The crystallization and melting behavior of PP in the composites were investigated by DSC. The experimental results showed that the crystallization temperature of PP in the composites increased with increasing nano-CaCO 3 content. Addition of PP-g-AA further increased the crystallization temperatures of PP in the composites. It is suggested that PP-g-AA could improve the nucleation effect of nano-CaCO 3 . However, the improvement in the nucleation effect of nano-CaCO 3 would be saturated when the PP-g-AA content of 5 phf (parts per hundred based on weight of filler) was used. The increase in the crystallization temperature of PP was observed by adding AA into the composites and the crystallization temperature of the composites increased with increasing AA content. It is suggested that the AA reacted with nano-CaCO 3 and the formation of Ca(AA) 2 promoted the nucleation of PP. In the presence of DCP, the increment of the AA content had no significant influence on the crystallization temperature of PP in the composites.
Inflammatory bowel disease is characterized with uncontrolled immune response in inflamed mucosa, with dominance of Th1 cells. Recently, all-trans retinoic acid has been shown that can lead T-cell response by suppressing Th17 development via retinoic acid receptor (RAR), but it is still unknown whether all-trans retinoic acid can modulate Th1 response of inflammatory bowel disease. In the experiment, we investigated the effect of all-trans retinoic acid on trinitrobenzene sulfonic acid (TNBS)-induced murine colitis, and the possible mechanism. Mice were intraperitoneally treated daily with all-trans retinoic acid (the agonist of RAR-alpha) or LE135 (the antagonist of RAR-alpha) or medium, and sacrificed 6 days later. Colon was collected for histological analysis and myeloperoxidase (MPO) activity measurement. Lamina propria mononuclear cells (LPMCs) were isolated, cultured, and assayed for the expressions of T-bet and GATA-3 by the use of Western blot and for cytokine levels by the use of ELISA. All-trans retinoic acid treatment inhibited inflammatory responses as shown by lower histological inflammatory scores and MPO activity, compared with LE135 and medium groups. Furthermore, in LPMCs culture supernatants, the levels of Th1 cytokines (INF-gamma, IL-12, and TNF-alpha) were decreased while those of Th2 cytokines (IL-4 and IL-10) were increased significantly in all-trans retinoic acid-treated mice. In addition, T-bet expression in LPMCs was inhibited and GATA-3 expression was up-regulated in all-trans retinoic acidtreated mice. On the contrary, LE135 showed the reverse effects in colon inflammation and cytokine profile. By shifting Th1 to Th2 profile in inflamed mucosa, all-trans retinoic acid down-regulates inflammatory response and ameliorates acute TNBS-induced colitis, which suggests the ligand of RAR-alpha-based pharmaceutical strategies for managing inflammatory bowel disease.
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