Epigallocatechin‐3‐gallate protected vanadium‐induced eggshell depigmentation via P38MAPK‐Nrf2/HO‐1 signaling pathway in laying hens

ABSTRACT It has been demonstrated that tea polyphenol (TP) epigallocatechin‐3‐gallate (EGCG) can confer protection against vanadium (V) toxicity in laying hens; however, our understanding of the molecular mechanisms beyond this effect are still limited. In this study, 360 hens were randomly assigned to the 3 groups to study whether the potential mechanism P38MAPK‐Nrf2/HO‐1 signaling pathway is involved in the protective effect of EGCG on eggshell pigmentation in vanadium challenged laying hens. Treatments included a control group, a 10 mg/kg V (V10), and a V10 plus 130 mg/kg of EGCG group (V10+EGCG130). Both eggshell color and protoporphyrin IX were decreased in the V10 group compared with the control diet, while EGCG130 treatment partially improved shell color and protoporphyrin IX (P < 0.05). The V10 exposure induced higher cell apoptosis rate and oxidative stress in birds as evidenced by the histological apoptosis status, decreased uterine glutathione‐S transferase (GST) and high abundance of malondialdehyde (MDA) compared with the control group, whereas EGCG130 markedly alleviated oxidative stress via reducing MDA generation (P < 0.05). Dietary vanadium reduced ferrochelatase, NF‐E2‐related factor 2 (Nrf2), and heme oxygenase (HO‐1) mRNA expression, while EGCG up‐regulated Nrf2 and HO‐1 expression (P < 0.05). Protein levels of Nrf2, HO‐1 and phospho‐p38 (P‐P38) MAPK were reduced in V10 group, while dietary supplementation with 130 mg/kg EGCG markedly increased Nrf2, HO‐1 and P‐P38 MAPK protein levels in the uterus compared with the V10 group (P < 0.01). In conclusion, EGCG improved eggshell color and antioxidant system in V10‐challenged hens, which seems to be associated with P38MAPK‐Nrf2/HO‐1 signaling pathway.

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