l-carnitine and fat type in the maternal diet during gestation and lactation modify the fatty acid composition and expression of lipid metabolism-related genes in piglets.

This study examined the influence of adding different amounts of maternal dietary l-carnitine and two fat types on fatty acid (FA) composition and the expression of lipid metabolism-related genes in piglets. The experiment was designed as a 2 × 2 factorial with two fat types (3.5% soyabean oil, SO, and 3.5% fish oil, FO) and two levels of l-carnitine (0 and 100 mg/kg) added to the sows' diets. A higher proportion of n-3 polyunsaturated fatty acids (PUFA) and a lower ratio of n-6/n-3 PUFA in sow milk and piglet tissues were observed in the FO groups than in the SO groups. Adding l-carnitine increased the proportion of C16:1 in sow milk and decreased n-3 PUFA in piglet subcutaneous fat. Hepatic peroxisome proliferator-activated receptor α (PPAR-α) was more abundantly expressed in piglets from the FO groups than from the SO groups (p < 0.05), whereas stearoyl-CoA-desaturase (SCD), sterol regulatory element binding protein-1 (SREBP1) and ∆6-desaturase (D6D) genes were less expressed in the FO groups compared with piglets from the SO groups. The expression of fatty acid synthase (FAS) genes was decreased in the SO groups with l-carnitine compared to that of the other dietary treatments. No differences among dietary treatments were observed with regard to the expression of acetyl-CoA carboxylase (ACC). In conclusion, FO and l-carnitine supplementation in sows affect FA composition and hepatic gene expression in piglets.

Icariin reduces human colon carcinoma cell growth and metastasis by enhancing p53 activities.

Icariin has been reported to possess high anticancer activity. Colon carcinoma is one of the leading causes of cancer-related mortality worldwide. Here, the anticancer activity of icariin against HCT116 colon carcinoma cells and the possible underlying mechanism were studied. The trypan blue staining assay, wound healing assay, clonogenic assay, CCK-8 assay, and Annexin V-FITC/PI double staining method were carried out to determine the changes of HCT116 cell growth and migration. mRNA and protein expressions were determined by quantitative real-time PCR and western blot, respectively. Moreover, small interfering RNA (siRNA) plasmid was used to examine the role of p53 in icariin-induced apoptosis in HCT116 cells. Icariin significantly suppressed colon carcinoma HCT116 cells by decreasing migration and viability, and simultaneously promoting apoptosis. Icariin exerted the anti-tumor effect in a dose-dependent manner by up-regulating p53. During treatment of icariin, p-p53, p21, and Bax levels increased, and Bcl-2 level decreased. Short time treatment with icariin induced DNA damage in HCT116 cells. Furthermore, the cytotoxicity of icariin was decreased after p53 knockdown or by using caspase inhibitors. p53 was involved in activities of caspase-9 and caspase-3. Icariin repressed colon carcinoma cell line HCT116 by enhancing p53 expression and activating p53 functions possibly through Bcl-2/Bax imbalance and caspase-9 and -3 regulation. Icariin treatment also induced DNA damage in HCT116 cells.

Icariin reduces human colon carcinoma cell growth and metastasis by enhancing p53 activities

Icariin has been reported to possess high anticancer activity. Colon carcinoma is one of the leading causes of cancer-related mortality worldwide. Here, the anticancer activity of icariin against HCT116 colon carcinoma cells and the possible underlying mechanism were studied. The trypan blue staining assay, wound healing assay, clonogenic assay, CCK-8 assay, and Annexin V-FITC/PI double staining method were carried out to determine the changes of HCT116 cell growth and migration. mRNA and protein expressions were determined by quantitative real-time PCR and western blot, respectively. Moreover, small interfering RNA (siRNA) plasmid was used to examine the role of p53 in icariin-induced apoptosis in HCT116 cells. Icariin significantly suppressed colon carcinoma HCT116 cells by decreasing migration and viability, and simultaneously promoting apoptosis. Icariin exerted the anti-tumor effect in a dose-dependent manner by up-regulating p53. During treatment of icariin, p-p53, p21, and Bax levels increased, and Bcl-2 level decreased. Short time treatment with icariin induced DNA damage in HCT116 cells. Furthermore, the cytotoxicity of icariin was decreased after p53 knockdown or by using caspase inhibitors. p53 was involved in activities of caspase-9 and caspase-3. Icariin repressed colon carcinoma cell line HCT116 by enhancing p53 expression and activating p53 functions possibly through Bcl-2/Bax imbalance and caspase-9 and -3 regulation. Icariin treatment also induced DNA damage in HCT116 cells.

Sphingosine kinase 1 as an anticancer therapeutic target.

The development of chemotherapeutic resistance is a major challenge in oncology. Elevated sphingosine kinase 1 (SK1) levels is predictive of a poor prognosis, and SK1 overexpression may confer resistance to chemotherapeutics. The SK/sphingosine-1-phosphate (S1P)/sphingosine-1-phosphate receptor (S1PR) signaling pathway has been implicated in the progression of various cancers and in chemotherapeutic drug resistance. Therefore, SK1 may represent an important target for cancer therapy. Targeting the SK/S1P/S1PR signaling pathway may be an effective anticancer therapeutic strategy, particularly in the context of overcoming drug resistance. This review summarizes our current understanding of the role of SK/S1P/S1PR signaling in cancer and development of SK1 inhibitors.

[Studies on extraction, isolation and composition of Lycium barbarum polysaccharides].

OBJECTIVE: To study the extraction, isolation and composition of Lycium barbarum polysaccharides (LBP). METHOD: LBP was extracted from L. barbarum with water, isolationed and purified by DEAE ion-exchange cellulose and gel chromatography, and their structural composition was studied by means of SDS-PAGE gel electrophoresis, GC, amino acid automatic analysis, etc. RESULT: Pure LBP has four water solubie polysaccharides, M W was 1.524 x 10(5). LBP was composed of 6 kinds of monosaccharides (Ara, Rha, Xyl, Man, Gal and Glc), galacturonic acid and 18 kinds of amino acids. CONCLUSION: LBP is a kind of complex polysaccharides consisting of acidic heteropolysaccharides and polypeptide or protein, and LBP has Glycan-O-Ser glycopeptide structures.