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Data · dataset · 2026

Gypenosides ameliorate heat stress-induced inflammatory injury in the bursa of Fabricius of broilers by activating the NF-κB signaling pathway

Listed in Teesside University Research Data Repository

Description

Data Description and Interpretation Experimental Subjects and Design This study selected a total of 200 broilers at 28 days of age, randomly divided into five groups (40 broilers per group), with the specific groupings as follows: CON (Control Group): Basal diet + Normal temperature (24 ± 1 ℃) HS (Heat Stress Group): Basal diet + High temperature (33 ± 1 ℃, 8 hours per day) HSLGP (Low-Dose Gypenoside Group): Basal diet + 200 mg/kg GP + High temperature HSMGP (Medium-Dose Gypenoside Group): Basal diet + 300 mg/kg GP + High temperature HSHGP (High-Dose Gypenoside Group): Basal diet + 450 mg/kg GP + High temperature Data Content and Collection

Method

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The data were derived from qPCR and Western Blot detection results of the bursa of Fabricius tissues from each group. Three samples were randomly selected from each group for analysis (reduced from the original plan of 8 samples to 3 for simplification). qPCR Data: The expression levels of genes related to inflammation and antioxidant defense (HO-1, ikba, nrf2, p65) were detected. WB Data: The expression levels of corresponding proteins (HO-1, IKBA, NRF2, P65) were measured.

Significant Findings Gene Expression: Compared with the CON group, p65 gene expression was significantly elevated in the HS group, indicating that heat stress activated the NF-κB inflammatory pathway. After GP supplementation (in HSLGP, HSMGP, and HSHGP groups), p65 expression was downregulated, while antioxidant genes such as nrf2 were upregulated, with the most pronounced effect observed in the HSHGP group. Protein Expression: The WB results were consistent with the qPCR trends.

P65 protein levels were elevated in the HS group and decreased after GP supplementation, while antioxidant proteins such as HO-1 showed increased expression. Data Interpretation Inflammation Regulation: GP alleviates heat stress-induced inflammatory responses by inhibiting p65 expression and blocking the NF-κB pathway. Antioxidant Effects: GP activates the Nrf2 pathway, promoting the expression of antioxidant proteins such as HO-1 and enhancing cellular defense against oxidative damage.

Dose-Dependent Effects: High-dose GP (HSHGP) demonstrated the best regulatory effects on gene and protein expression, suggesting that GP's anti-inflammatory and antioxidant actions may exhibit dose dependency.

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