epidermal-growth-factor has been researched along with Swine-Diseases* in 4 studies
2 trial(s) available for epidermal-growth-factor and Swine-Diseases
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Effects of dietary epidermal growth factor supplementation on liver antioxidant capacity of piglets with intrauterine growth retardation.
The present experiment was conducted to study the effects of dietary epidermal growth factor (EGF) supplementation on the liver antioxidant capacity of piglets with intrauterine growth retardation (IUGR). The present study consists of two experiments. In experiment 1, six normal-birth-weight (NBW) and six IUGR newborn piglets were slaughtered within 2 to 4 h after birth to compare the effects of IUGR on the liver antioxidant capacity of newborn piglets. The results showed that compared with NBW piglets, IUGR piglets had a lower birth weight and liver relative weight; IUGR piglets had a higher serum malondialdehyde (MDA) level, liver MDA level and hydrogen peroxide (H2O2) level, and had a lower liver total antioxidant capacity (T-AOC) level and glutathione peroxidase (GSH-Px) activity; IUGR trended to increase serum alanine aminotransferase activity, aspartate aminotransferase activity, and H2O2 level, and trended to decrease liver total superoxide dismutase activity. In experiment 2, six NBW piglets, and 12 IUGR piglets weaned at 21 d of age were randomly divided into the NC group (NBW piglets fed with basal diet); IC group (IUGR piglets fed with basal diet), and IE group (IUGR piglets fed with basal diet plus 2 mg/kg EGF), and feeding for 14 d. Organ index, serum parameters, liver antioxidant capacity, and liver antioxidant-related genes expression were measured. The results showed that compared to the IC group, dietary EGF supplementation (IE group) significantly reduced serum malondialdehyde level and H2O2 level, and liver protein carbonyl (PC) level and 8-hydroxydeoxyguanosine level of piglets with IUGR; dietary EGF supplementation (IE group) significantly increased serum T-AOC level, liver T-AOC level and GSH-Px activity; dietary supplemented with EGF (IE group) enhanced liver Nrf2, NQO1, HO1, and GPX1 mRNA expression compared to IC group. Pearson's correlation analysis further showed that EGF can alleviate liver oxidative injury caused by IUGR and improve the performance of IUGR piglets. In conclusion, EGF exhibited potent protective effects on IUGR-induced liver oxidative injury, by activating the Nrf2 signaling pathway to mediate the expression of downstream antioxidant enzymes and phase II detoxification enzymes (NQO1 and HO1), thereby alleviating liver oxidative damage and promoting the growth performance of IUGR piglets.. The liver is an important metabolic and secretory organ in vertebrates, which plays an important role in the overall health of animals. Studies have shown that intrauterine growth retardation (IUGR) can cause liver injury in piglets, which is unfavorable to the growth and development of piglets. Epidermal growth factor (EGF) has antioxidant properties, but its effect on liver oxidative damage caused by IUGR remains uncertain. In the present study, we chose newborn piglets with low birth weight as the IUGR models to investigate whether IUGR could cause oxidative damage in the liver. Then, the diet supplemented with EGF was fed to IUGR piglets to study the effects of EGF supplementation on the liver antioxidant function of IUGR-weaned piglets. Results showed that IUGR caused serious damage to the liver of piglets, while dietary EGF supplementation could reverse the oxidative injury induced by IUGR to some extent. Therefore, this study confirmed that EGF has positive effects on the liver health of piglets with IUGR. Topics: Animals; Antioxidants; Dietary Supplements; Epidermal Growth Factor; Female; Fetal Growth Retardation; Hydrogen Peroxide; Liver; Malondialdehyde; NF-E2-Related Factor 2; Swine; Swine Diseases | 2023 |
Heat-stress-induced damage to porcine small intestinal epithelium associated with downregulation of epithelial growth factor signaling.
Extreme heat during certain days of the summer renders pigs susceptible to severe heat stress, which negatively affects their growth performance. We hypothesized that such heat stress impaired the small intestinal mucosa, a site responsible for nutrient absorption. To simulate heat stress, Chinese experimental mini-pigs were treated with 5 h of continual 40 degrees C temperature each day for 10 d in succession. Pigs were killed at 1, 3, 6 and 10 d after treatment, and small intestinal epithelia were sampled for histochemical examination and biochemical analyses. The duodenum and jejunum were seriously damaged within 3 d of initiation of treatment. Subsequent study of the process of jejunum recovery showed that the initiation of recovery started within 6 d following heat stress. Such damage was associated with the downregulation of epithelial growth factor signaling. In conclusion, heat stress induced short-term damage to the epithelium of porcine intestine. Because the intestinal epithelium is crucial for nutrient uptake, such damage should partially account for the impairment of growth performance of pigs under heat stress. Topics: Animals; DNA; Epidermal Growth Factor; ErbB Receptors; Gene Expression Regulation; Heat Stress Disorders; Intestinal Diseases; Intestinal Mucosa; Jejunum; Male; Swine; Swine Diseases; Time Factors | 2009 |
2 other study(ies) available for epidermal-growth-factor and Swine-Diseases
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A mouse model study for the villous atrophy of the early weaning piglets.
Early weaning induces villous atrophy in the small intestine of piglets. We evaluated an influence of early weaning at 16 days old in mice for the use of villous atrophy model observed in early-weaned piglets. Five pregnant BALB/c mice were obtained and half of pups were weaned at 16 days old (early-weaned), while the others were allowed to suckle. Their small intestine was collected at 17, 18 and 19 days old in each group. Villous was shorting at 17 and 18 days old, but obscured at 19 days old. The gene expressions of epidermal and platelet-derived growth factor were associated with the villous height. Early weaning induced villous atrophy in the mouse small intestine as well as the piglets. Topics: Animals; Animals, Newborn; Atrophy; Disease Models, Animal; DNA; Epidermal Growth Factor; Female; Histocytochemistry; Intestinal Diseases; Intestinal Mucosa; Mice; Mice, Inbred BALB C; Platelet-Derived Growth Factor; Polymerase Chain Reaction; Swine; Swine Diseases | 2010 |
Expression of tumor necrosis factor-alpha and cyclooxygenase-2 mRNA in porcine split-thickness wounds treated with epidermal growth factor by quantitative real-time PCR.
Epidermal growth factor (EGF) accelerates the re-epithelialization of damaged epidermal cell layers in a wound, so it especially shortens the duration of wound healing. The effect of EGF on pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and cyclooxygenase-2 (COX-2), levels during wound healing has not been reported. We investigated the relationship between exogenous EGF treatment and the expression of TNF-alpha and COX-2 mRNA in porcine split-thickness wounds by real-time PCR. Twenty split-thickness wounds were created on the back of five pigs. Fifteen wounds were treated twice daily with EGF ointments (1 microg/g, 10 microg/g, and 50 microg/g) for 10 days and five wounds were untreated. Healing time until full-epithelialization was evaluated. We performed a quantitative analysis of TNF-alpha and COX-2 mRNA expression in wound biopsies using real-time PCR. Topical application of 1 microg/g EGF accelerated re-epithelialization more than treatments of EGF at 10 microg/g and 50 microg/g, and no treatment. The levels of TNF-alpha and COX-2 mRNA were significantly greater in wounds treated with 1 microg/g than those with 10 microg/g and 50 microg/g EGF, and no treatment. Topical treatment of EGF influences the level of TNF-alpha and COX-2 mRNA within porcine split-thickness wounds. EGF-dependent slightly up-regulation of TNF-alpha and COX-2 mRNA expression during the inflammatory phase of healing may create an optimal molecular environment for wound healing. Topics: Animals; Cyclooxygenase 2; Dose-Response Relationship, Drug; Epidermal Growth Factor; Gene Expression Regulation; Polymerase Chain Reaction; RNA, Messenger; Swine; Swine Diseases; Tumor Necrosis Factor-alpha; Wound Healing; Wounds and Injuries | 2007 |