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Via an assay using an Amino Acid Analyzer, pepsin-digested chicken liver hydrolysates (CLHs) contain taurine (365.57 ± 39.04 mg/100 g), carnosine (14.03 ± 1.98 mg/100 g), and anserine (151.58 ± 27.82 mg/100 g). This study aimed to evaluate whether CLHs could alleviate thioacetamide (TAA)-induced fibrosis. A dose of 100 mg TAA/kg BW significantly increased serum liver damage indices and liver cytokine contents. Cell infiltration and monocytes/macrophages in livers of TAA-treated rats were illustrated by the H&E staining and immunohistochemical analysis of cluster of differentiation 68 (CD68, ED1), respectively. A significantly increased hepatic collagen accumulation was also observed and quantified under TAA treatment. A significant up-regulation of transforming growth factor-beta (TGF-β) and SMAD family member 4 (SMAD4) caused by TAA treatment further enhanced alpha smooth muscle actin (αSMA) gene and protein expressions. The liver antioxidant effects under TAA treatment were significantly amended by 200 and 600 mg CLHs/kg BW. Hence, the ameliorative effects of CLHs on liver fibrogenesis could be attributed by antioxidation and anti-inflmmation.

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This study aims to clarify the effects of chicken liver hydrolysates (CLHs) on long-term high-fat diet (HFD)-induced insulin resistance (IR) and hepatosteatosis in mice. In vitro , the 400 μM oleic acid (OA)-added medium successfully stimulated the cellular steatosis on FL83B cells, and the cellular steatosis was attenuated ( p < 0.05) by supplementing with CLHs (4 mg/L). In vivo , the effects of CLHs on IR and hepatosteatosis development were tested in 20-week HFD-fed mice. HFD-induced increases in final body weight, but body weight gains of mice were decreased ( p < 0.05) by supplementing CLHs. Elevated ( p < 0.05) serum aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), free fatty acids (FFAs), triglyceride (TG), total cholesterol (TC), and fasted glucose values in HFD-fed mice decreased ( p < 0.05) by supplementing CLHs. Both results of hepatic steatosis and fibrotic scores also indicated the retardation ( p < 0.05) of the hepatosteatosis in cotreated groups. Moreover, the CLH supplementation sustained ( p < 0.05) hepatic and peripheral insulin signal sensitivity in HFD-fed mice. CLH supplementation could ameliorate hepatic lipid deposition, hepatic/peripheral IR in a long-term high-fat dietary habit, and also improve the universal glucose homeostasis by upregulating hepatic and peripheral insulin sensitivities.

BACKGROUND: Reactive oxygen species (ROS) overproduction is highly related to some human chronic diseases. There are approximately 400 metric tons of chalazae produced yearly after the processing of the liquid-egg production, which are disposed of as waste. The objectives of this study were to look for the optimal production condition of antioxidant crude chalaza hydrolysates and evaluate the in vivo antioxidant capacity via a chronic alcohol consumption mouse model. RESULTS: Antioxidant crude chalaza hydrolysates (CCH-As) could be produced by proteaseA at 1:100 ratio (w/w) and 0.5 h hydrolytic period. After our analyses, CCH-As were rich in leucine, arginine, phenylalanine, valine, lysine and antioxidant dipeptides (anserine and carnosine), and the major molecular masses were lower than 15 kDa. Regarding protective effects of CCH-As against oxidative damage in alcoholic-liquid-diet-fed mice, alcohol-fed mice had lower (P < 0.05) liver antioxidant capacities, and higher (P < 0.05) liver lipid contents, serum lipid/liver damage indices and IL-1 /IL-6 values. CCH-A supplementation reversed (P < 0.05) liver antioxidant capacities and reduced (P < 0.05) serum/liver lipids in alcohol-fed mice, which may result from increased (P < 0.05) fecal lipid output, upregulated (P < 0.05) fatty acid -oxidation and downregulated (P < 0.05) lipogenesis in the liver. CONCLUSION: Taken together, this CCH-A should benefit the liquid-egg industry, while also offering consumers a choice of healthy ingredients from animal sources.Keywords: alcoholic fatty liver; amino acid profile; in vitro and in vivo antioxidant effects; lipid metabolism; protease-A-digested crude chalaza hydrolysate Industry and 0.25 mL potassium ferricyanide (1%) (Sigma Co.), and the mixture was incubated at 50 ∘ C for 15 min. 0.25 mL trichloroacetic acid solution (10%) (Sigma Co.) was added to the mixture, which was then centrifuged at 900 × g for 10 min at room temperature. Then J Sci Food Agric 2019; 99: 2300-2310In vivo hepatoprotective effects of CCH-As Effects of CCH-As on body weight, size of organs and abdominal fat pad, serum biochemical values, liver damage status, and hepatic and fecal lipids in chronic alcohol-fed mice With regard to an in vivo antioxidant effect of our manufactured CCH-As, chronic alcoholic liquid-diet-fed mice were applied as J Sci Food Agric 2019; 99: 2300-2310

Thioacetamide (TAA), usually used as a fungicide to control the decay of citrus products, itself is not toxic to the liver, but its intermediates are able to increase oxidative stress in livers and further cause fibrosis. Ophiocordyceps sinensis mycelium (OSM) which contains 10% polysaccharides and 0.25% adenosine decreased (P < 0.05) the lipid accumulation and increased (P < 0.05) antioxidative capacity in livers of thioacetamide (TAA) injected rats. Meanwhile, the increased (P < 0.05) liver sizes, serum alanine transaminase (AST) and aspartate transaminase (ALT) values in thioacetamide (TAA)-injected rats were ameliorated (P < 0.05) by OSM supplementation. Moreover, the levels of proinflammatory cytokines, such as the tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), were also reduced (P < 0.05). The fibrosis phenomena in pathological (Masson's trichrome and H&E stainings) and immunohistochemical [α-smooth actin (αSMA) and CD86/ED1] observations in TAA-treated rats were reduced (P < 0.05) by OSM cotreatment. The protective effect of OSM against TAA-induced liver inflammation/fibrosis may be via downregulations (P < 0.05) of TGF-β pathways and NFκB which further influenced (P < 0.05) the expressions of fibrotic and inflammatory genes (i. e., αSMA, Col1α, COX2). Therefore, OSM shows preventive effects on the development of TAA-induced hepatic fibrosis.

Our patented protease A–digested crude chalaza hydrolysates ( CCH ) show antioxidant abilities in vitro. The prophylactic effects of CCH on cognitive dysfunction and brain oxidative damages were investigated via a D-galactose ( DG )–injected mouse model in this study. Fifty-four mice were randomly divided into the following: (1) CON, 0.1 mL 0.9% saline (subcutaneous injection [ SC ] on the back)+distilled water (oral gavage); (2) DG, 100 mg/kg BW/day D-galactose (Bio-Serv Co., Flemington, NJ, USA) (SC on the back)+distilled water (oral gavage); (3) DG_LCH, 100 mg/kg BW/day D-galactose (SC on the back) + 50 mg CCH/kg BW/day in 0.1 ml distilled water (oral gavage); (4) DG_MCH, 100 mg/kg BW/day D-galactose (SC on the back) + 100 mg CCH/kg BW/day (oral gavage); (5) DG_HCH, 100 mg/kg BW/day D-galactose (SC on the back) + 200 mg CCH/kg BW/day (oral gavage); (6) DG_AG, 100 mg/kg BW/day D-galactose (SC on the back) + 100 mg aminoguanidine hydrochloride/kg BW/day (oral gavage). The experiment lasted for 84 D. CCH, containing antioxidant-free amino acids and anserine, restored ( P < 0.05) DG-injected memory injury in the Morris water maze test and attenuated the neuronal degenerations and nucleus shrinkages in the dentate gyrus area. CCH supplementation also reduced amyloid β-peptide protein levels and accumulation of advanced glycation end products (AGE) in the brain of DG-injected mice, whereas the brain antioxidant capacity was reversed ( P < 0.05) by supplementing CCH. Furthermore, AGE receptor ( RAGE ), NFκb , IL-6 , and TNF-α gene expressions were downregulated ( P < 0.05) by supplementing CCH. Therefore, CCH show prophylactic effects on the development of oxidative stress-induced cognitive dysfunction.

Salmonellosis in broilers is not merely a significant disease with high economic costs in the poultry industry but also the foodborne disease with the impact on public health by cross-contamination. This study was to investigate the prebiotic ability of trehalose supplementing in diets (0, 1, 3, and 5%, w/w) against Salmonella by using S. Typhimurium ( ST )-inoculated broilers. The improvements ( P < 0.05) of feed conversion ratio ( FCR ) were observed with 5% trehalose supplementation in ST-inoculated broilers' diets. An addition of 3 or 5% trehalose in diets increased ( P < 0.05) the abundance of lactobacilli in the duodenum and jejunum but decreased ( P < 0.05) the growth of ST in the cecum. The adverse effects on serum levels of aspartate aminotransferase, triglyceride, and albumin and globulin ratio in ST-inoculated broilers were noticed and counteracted by supplementing 3 or 5% trehalose in diets ( P < 0.05). Besides, the inclusion of trehalose in diets alleviated the intestinal damages and maintained the integrity of cecal epithelial cells after ST challenge under an haematoxylin and eosin-staining observation. Supplementing trehalose further showed the inhibitions of toll-like receptor 4-mediated nuclear factor-kappa-B pathway, including the downregulation ( P < 0.05) of proinflammatory cytokine genes, such as interleukin 1 beta and lipopolysaccharide-induced tumor necrosis factor-alpha factor and the upregulation ( P < 0.05) of interleukin 10 and interferon-alpha in ST-inoculated broilers. Overall, supplementing trehalose alleviated the adverse effects from ST challenge on FCR, serum biochemistry, the damage, and inflammation in the liver and cecum. Those improvements on ST challenged broilers also contributed to the overgrowth of lactobacilli, the decrement of ST, and anti-inflammatory effects in affected broilers. Trehalose, therefore, could be a promising prebiotic against salmonellosis to benefit broiler production and promote food safety in the poultry industry.