Effects of Lecithin Supplementation in Feed of Different fat Levels on Serum Indexes and Liver Health of Laying Hens.

The aim of this experiment was to investigate the effect of soy lecithin on serum-related indicators and liver health in laying hens under the influence of high-fat diets. 180 peak laying hens at 40 weeks of age were randomly assigned to one of the four diets using a 2 × 2 factorial and fed for 5 weeks. The results showed that compared to the low-fat group, the high-fat group had lower egg production (p < 0.05) and higher average daily feed intake and feed-to-egg ratio (p < 0.05). At the 21st day, the serum levels of triglyceride (TC) and superoxide dismutase (SOD) were higher (p < 0.05), high-density lipoproteins cholesterol (HDL-C) levels were lower (p < 0.01), catalase (CAT) activity was lower (p < 0.05), TC and malondialdehyde (MDA) levels in liver were higher (p < 0.01) and SOD activity in liver was lower (p < 0.05) in layers supplemented with soy lecithin. CAT activity in serum was increased (p < 0.01) and total antioxidant capacity (T-AOC) activity in the liver was decreased (p < 0.05) after increasing the dietary fat concentration. The addition of soy lecithin and the increase in dietary fat concentration had a highly significant interaction on serum CAT activity and liver TC content in layers (p < 0.01). At the 35th day, the serum alanine aminotransferase (ALT) activity was higher (p < 0.01), serum glutathione peroxidase (GSH-Px) and CAT activity were higher (p < 0.05), and serum triglyceride (TG) content and total T-AOC capacity activity were lower (p < 0.05) in layers supplemented with soy lecithin. Increasing dietary fat concentration decreased alanine aminotransferase (ALT), aspartate aminotransferase (AST) and GSH-Px activity in serum (p < 0.05). However, it increased TG and MDA content in liver (p < 0.05), and highly decreased SOD content in liver (p < 0.01) in layers. The addition of soy lecithin and increasing dietary fat concentration had a highly significant reciprocal effect on serum ALT viability and CAT viability (p < 0.01) and liver TG and MDA content and SOD viability (p < 0.05) in layers. In conclusion, feeding high-fat diets will adversely affect the laying performance of laying hens, while long-term addition of lecithin can improve the blood lipids and liver lipids of laying hens, enhance the antioxidant capacity of the liver, and maintain liver health.

The preventive effect and mechanisms of adsorbent supplementation in low concentration aflatoxin B1 contaminated diet on subclinical symptom and histological lesions of broilers.

This study aimed to investigate the subclinical symptom and histological lesions of 21-day-old and 42-day-old broilers exposure to low concentration aflatoxin B1 (AFB1), and the preventive effect with adsorbent (Toxo-MX) supplementation. A total of 576 one-day-old Arbor Acres broilers were randomly allotted into 6 treatments 8 replicates and 12 birds per cage, fed with 0 ppb, 60 ppb and 120 ppb AFB1 contamination diet with or without Toxo-MX supplementation. Results showed both 60 ppb and 120 ppb AFB1 contamination significantly reduced growth performance in 21-day-old broilers (P < 0.05), but not in 42-day-old broilers (P > 0.05), however, AFB1 contamination in diet caused a higher feed to gain ratio (P < 0.05). Broilers of 21-day-old exposure to 60 ppb and 120 ppb AFB1 increased mRNA expression of hepatic inflammatory cytokines, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activity (P < 0.05), 42-day-old broilers showed a same change in 120 ppb but not in 60 ppb of AFB1 contamination (P < 0.05). mRNA expressions of clauding-1, Zonula occludens-1 (ZO-1), and occludin decreased, but Bax, Bcl-2, and caspase-3 increased in 21-day-old broilers exposure to 60 ppb and 120 ppb AFB1 (P < 0.05), broilers of 42-day-old resisted on intestinal aflatoxicosis impairment against 60 ppb AFB1 contamination (P < 0.05), but not in 120 ppb (P < 0.05). Toxo-MX supplementation significantly reversed the detrimental effects on growth performance in both age broilers and reduced the accelerated feed to gain ratio caused by AFB1 (P < 0.05). Intestinal mRNA expression of tight junction and apoptotic genes in both age broilers were recovered by Toxo-MX supplementation (P < 0.05). However, Toxo-MX did not restore the accelerated expression of hepatic inflammation cytokines and SOD, GSH-Px in 120ppb AFB1 group (P < 0.05). The data demonstrated that diet supplementation with Toxo-MX reversed the detrimental effect on growth performance and intestine in broilers exposure to 60 ppb and 120 ppb AFB1. However, did not completely recovered hepatic inflammation induced by AFB1.

Correction to: Adenovirus-mediated LIGHT gene modification in murine B-cell lymphoma elicits a potent antitumor effect.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Hispidin induces autophagic and necrotic death in SGC-7901 gastric cancer cells through lysosomal membrane permeabilization by inhibiting tubulin polymerization.

Hispidin and its derivatives are widely distributed in edible mushrooms. Hispidin is more cytotoxic to A549, SCL-1, Bel7402 and Capan-1 cancer cells than to MRC5 normal cells; by contrast, hispidin protects H9c2 cardiomyoblast cells from hydrogen peroxide-induced or doxorubicin-induced apoptosis. Consequently, further research on how hispidin affects normal and cancer cells may help treat cancer and reduce chemotherapy-induced side effects. This study showed that hispidin caused caspase-independent death in SGC-7901 cancer cells but not in GES-1 normal cells. Hispidin-induced increases in LC3-II occurred in SGC-7901 cells in a time independent manner. Cell death can be partially inhibited by treatment with ATG5 siRNA but not by autophagy or necroptosis inhibitors. Ultrastructural evidence indicated that hispidin-induced necrotic cell death involved autophagy. Hispidin-induced lysosomal membrane permeabilization (LMP) related to complex cell death occurred more drastically in SGC-7901 cells than in GES-1 cells. Ca2+ rather than cathepsins from LMP contributed more to cell death. Hispidin induced microtubule depolymerization, which can cause LMP, more drastically in SGC-7901 cells than in GES-1 cells. At 4.1 µM, hispidin promoted cell-free tubulin polymerization but at concentrations higher than 41 µM, hispidin inhibited polymerization. Hispidin did not bind to tubulin. Alterations in microtubule regulatory proteins, such as stathmin phosphorylation at Ser16, contributed to hispidin-induced SGC-7901 cell death. In conclusion, hispidin at concentrations higher than 41 µM may inhibit tubulin polymerization by modulating microtubule regulatory proteins, such as stathmin, causing LMP and complex SGC-7901 cell death. This mechanism suggests a promising novel treatment for human cancer.

Magnolol additive as a replacer of antibiotic enhances the growth performance of Linwu ducks.

Magnolol rich in Magnolia officinalis is a bioactive polyphenolic compound. The aim of this study was to examine the effects of magnolol additive (MA) on growth performance, expression levels of antioxidant-related genes, and intestinal mucosal morphology of Linwu ducks aged from 49 to 70 days, comparing with that of an antibiotic additive (colistin sulfate [CS]). A total of 275, 49-day-old ducks were assigned to 5 groups with 5 cages of 11 ducks each and fed diets supplemented with 0, 100, 200 and 300 mg of MA/kg and 300 mg of CS/kg for 3 weeks, respectively. The results showed that the average daily body weight gain (ADG) was increased significantly in MA-fed groups (200 and 300 mg/kg), compared with the basal diet (BD) group (P < 0.05). The mRNA levels of superoxide dismutase-1 (SOD1), manganese superoxide dismutase-2 (MnSOD2) and catalase (CAT) were also increased significantly in MA groups (P < 0.05). In addition, hematoxylin and eosin staining revealed that Linwu ducks fed the diets with MA had more intact intestinal mucosa than those fed the BD and CS diets. In addition, ileal villus height, ileal villus height/crypt depth ratio (V/C) and duodenal V/C were also improved significantly (P < 0.05). Taken together, these data demonstrated that MA is an effective feed additive to enhance the growth performance of the Linwu ducks by improving the antioxidant and intestinal mucosal status, suggesting that MA will be a potential additive to replace antibiotic (CS).

Adenovirus-mediated LIGHT gene modification in murine B-cell lymphoma elicits a potent antitumor effect.

Here, we investigated the antitumor effect of adenovirus-mediated gene transfer of LIGHT, the tumor-necrosis factor (TNF) superfamily member also known as TNFSF14, in the murine A20 B-cell lymphoma. LIGHT gene modification resulted in upregulated expression of Fas and the accessory molecule--intercellular adhesion molecule-1 (ICAM-1) on A20 cells and led to enhanced A20 cell apoptosis. LIGHT-modified A20 cells effectively stimulated the proliferation of T lymphocytes and interferon (IFN)-gamma production in vitro. Immunization of BALB/c mice with a LIGHT-modified A20 cell vaccine efficiently elicited protective immunity against challenge with the parental tumor cell line. Adenovirus-mediated gene transfer of LIGHT by intratumoral injection exerted a very potent antitumor effect against pre-existing A20 cell lymphoma in BALB/c mice. This adenovirus-mediated LIGHT therapy induced substantial splenic natural killer (NK) and cytotoxic T lymphocyte (CTL) activity, enhanced tumor infiltration by inflammatory cells and increased chemokine expression of CC chemokine ligand 21 (CCL21), IFN-inducible protein-10 (IP-10) and monokine induced by IFN-gamma (Mig) from tumor tissues. Thus, adenovirus-mediated LIGHT therapy might have potential utility for the prevention and treatment of B-cell lymphoma.

EBAG9 inducing hyporesponsiveness of T cells promotes tumor growth and metastasis in 4T1 murine mammary carcinoma.

The estrogen receptor-binding fragment-associated gene 9 (EBAG9) has been identified as an estrogen-responsive gene and was recently identified as a tumor-promoting and prognostic factor for renal cell carcinoma. We investigated whether EBAG9 expression was correlated with primary tumor growth and distant tumor metastasis in a murine breast carcinoma model. Knockdown expression of EBAG9 by small interfering RNA significantly suppressed tumor growth and metastasis in vivo in a highly malignant, spontaneously metastasizing 4T1 mouse mammary carcinoma model. 4T1 cells stably overexpressing EBAG9 developed larger and faster tumor growth and lung metastasis compared with parental 4T1 or 4T1 expressing vector alone. Strong specific cytotoxic T lymphocyte activity and enhanced gamma-interferon and interleukin-2 productions were induced in mice that received EBAG9 small interfering RNA therapy. Gene silencing of EBAG9 prolonged the survival of tumor-bearing mice and induced more intensive infiltration of CD8+ T cells in tumor mass. EBAG9 induced apoptosis of T cells, enhanced glycogen synthase kinase 3beta phosphorylation and inhibited gamma-interferon production of T cells when T lymphocytes were cocultured with 4T1 cells overexpressing EBAG9. Furthermore, overexpression of EBAG9 in 4T1 cells was accompanied with enhanced expression of chemokine (C-X-C motif) receptor 4, which might be involved in tumor metastasis. Taken together, our results suggested that EBAG9 promoted primary 4T1 mammary carcinoma growth and distant metastasis, and EBAG9 small interfering RNA exerted overt regression of tumor growth and metastasis. These findings might provide insights into the mechanism through which tumors evade immunosurveillance and provide a strategy for therapeutic intervention of cancer metastases.