A study using 144 one-day-old Arbor Acres broilers was conducted to assess the effects of dried ginger root (Zingiber officinale) that was processed to particle sizes of 300, 149, 74, 37, and 8.4 microm on growth performance, antioxidant status, and serum metabolites of broiler chickens. The birds were housed in 24 wire cages in an environmentally controlled room. Dietary treatments were no supplementation (control) and supplementation with ginger root processed to 5 particle sizes at the level of 5 g/kg of diet. Average daily gain, ADFI, and feed conversion rate of chicks of each cage were measured weekly. Blood samples from 8 broilers per treatment were obtained at d 21 and 42 of the experiment to determine antioxidant enzymatic activities and metabolites in the serum, and the birds were subsequently killed to determine carcass yield and abdominal fat content. All broilers had similar ADFI or feed conversion rate over the entire experimental period. However, broilers supplemented with ginger powder tended to have higher ADG and had greater (P=0.014) carcass yield compared with that of the control. Supplementation of ginger increased (P<0.001) activities of total superoxide dismutase and glutathione peroxidase but reduced (P<0.01) concentrations of malondialdehyde and cholesterol in serum of broilers at 21 and 42 d of age. Concentration of total protein in serum of ginger-supplemented broilers tended (P=0.092) to be higher at 21 d and was higher (P=0.002) at 42 d of age compared with that of control broilers. Reducing particle size of ginger powder linearly reduced (P<0.05) cholesterol (d 21) and linearly increased (P<0.05) glutathione peroxidase (d 21), total superoxide dismutase (d 42), and total protein (d 21 and 42). Supplementation of ginger at the level of 5 g/kg improved antioxidant status of broilers and the efficacy was enhanced as the particle size was reduced from 300 to 37 microm.

Zearalenone (ZEA), an estrogenic mycotoxin, is produced mainly by Fusarium fungi. Previous studies indicated that acute ZEA exposure induced oxidative stress and damage in multiple organs. Therefore, the present study was designed to investigate the adverse effects of dietary ZEA (1.1 to 3.2 mg/kg of diet) on oxidative stress and organ damage in postweaning gilts. A total of 20 gilts (Landrace × Yorkshire × Duroc) weaned at d 21 with an average BW of 10.36 ± 1.21 kg was used in the study. Gilts were housed in a temperature-controlled room, divided into 4 treatments, and fed a basal diet only (control) or basal diet supplemented with purified ZEA at a dietary concentration of 1 (ZEA1), 2 (ZEA2), or 3 (ZEA3) mg/kg of diet for 18 d ad libitum. The actual ZEA contents (analyzed) were 0, 1.1 ± 0.02, 2.0 ± 0.01, and 3.2 ± 0.02 mg/kg for control, ZEA1, ZEA2, and ZEA3, respectively. Gilts fed different amounts of dietary ZEA grew similarly with no difference (P > 0.05) in feed intake. Vulva size increased linearly over the 18 d of feeding in gilts fed diets containing 1.1 mg of ZEA/kg or greater (P < 0.001). Relative weight of genital organs, liver, and kidney increased linearly (P < 0.05) in a ZEA-dose-dependent manner. Serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, γ-glutamate transferase, urea, and creatinine (P < 0.05), and malondialdehyde concentrations in both serum and liver (P < 0.001) were also increased linearly in a ZEA-dose-dependent manner. However, spleen relative weight (P = 0.002) and activities of total superoxide dismutase and glutathione peroxidase (in both serum and liver (P < 0.05) were decreased linearly as dietary ZEA increased. Results showed that besides genital organs, the liver, kidney, and spleen may also be target tissues in young gilts fed diets containing 1.1 to 3.2 mg of ZEA/kg for 18 d. Increased key liver enzymes in the serum suggest progressive liver damage caused by feeding ZEA, and an increase in oxidative stress in gilts is another potential impact of ZEA toxicity in pigs.

To investigate the effects of ginger root (Zingiber officinale) on laying performance and antioxidant status of laying hens and on dietary oxidation stability, 675 Hy-Line brown laying hens at 27 wk of age were randomly allocated to 5 treatments with 5 replicates in a complete randomized design. Laying hens were fed corn-soybean meal based diets and supplemented with 0, 5, 10, 15, or 20 g of ginger powder/kg of diet for 10 wk. The ADFI, laying rate, average egg weight, egg mass, and feed conversion of each replicate were measured weekly. Blood samples from 10 laying hens and 15 egg samples/treatment were obtained on d 35 and 70 of the experiment to determine the serum or egg yolk antioxidant enzymatic activities. Three separate batches of each treatment diet were also made at the beginning of the experiment and stored at 20°C. Subsamples were taken at 10-d intervals to determine the dietary oxidation stability over a 60-d period. All laying hens had similar ADFI, laying rate, average egg weight, and feed conversion. However, laying hens supplemented with ginger powder had higher (P = 0.024) egg mass than the control group. Supplementation of ginger powder increased (P < 0.05) the serum and egg yolk antioxidant enzymatic activities of laying hens on d 35 and 70. Increasing ginger powder from 0 to 20 g/kg of diet linearly increased (P < 0.05) the peroxide value but linearly reduced (P < 0.05) the acid value of lipid extracted from stored diets for the first 30 d, but not for the second 30 d. Dietary supplementation of ginger powder improved laying performance and serum and egg yolk antioxidant status and enhanced dietary oxidation stability in a dose-dependent manner. The optimum supplementation rate of ginger powder in the diet of laying hens appeared to be between 10 and 15 g/kg of diet.

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Berberine, an important protoberberine isoquinoline alkaloid, has several pharmacological activities, including antimicrobial, glucose- and cholesterol-lowering, antitumoral, and immunomodulatory properties. Substantial studies suggest that berberine may be beneficial to Alzheimer’s disease (AD) by limiting the pathogenesis of extracellular amyloid plaques and intracellular neurofibrillary tangles. Increasing evidence has indicated that berberine exerts a protective role in atherosclerosis related to lipid- and glucose-lowering properties, implicating that berberine has the potential to inhibit these risk factors for AD. This review also attempts to discuss the pharmacological basis through which berberine may retard oxidative stress and neuroinflammation to exhibit its protective role in AD. Accordingly, berberine might be considered a potential therapeutic approach to prevent or delay the process of AD. However, more detailed investigations along with a safety assessment of berberine are warranted to clarify the role of berberine in limiting these risk factors and AD-related pathologies.

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