Cadmium (Cd) can cause endoplasmic reticulum stress (ERS) and apoptosis in animals. The kidney is an organ seriously affected by Cd because it can accumulate
metal ions.
Astilbin (ASB) is a dihydroflavonol rhamnoside, which has an anti-renal injury effect. This study aimed to evaluate the protective effect of ASB on Cd-induced ERS and apoptosis in the chicken kidney. In this study, a total of 120 1-day-old chickens were randomly divided into 4 groups. Chickens were fed with a basic diet (Con group), ASB 40 mg/kg (ASB group),
CdCl2 150 mg/kg + ASB 40 mg/kg (ASB/Cd group), and
CdCl2 150 mg/kg (Cd group) for 90 days. The results showed that Cd exposure induced pathological and ultrastructural damages and apoptosis in chicken kidneys. Compared with the Con group,
metallothionein (MT1/MT2) level,
nitric oxide (NO) content,
inducible nitric oxide synthase (iNOS) activity, ERS-related genes 78-kDa
glucose-regulated
protein (
Grp78),
protein kinase PKR-like endoplasmic reticulum
kinase (Perk),
activating transcription factor 4 (Atf4) and
CAAT/enhancer-binding protein (
C/EBP) homologous protein (Chop), and pro-apoptotic gene
B-cell lymphoma 2 (Bcl-2)-associated X (Bax),
caspase-12,
caspase-9,
caspase-3 expression levels, and apoptotic rate were significantly increased in the Cd group. The expression level of Bcl-2 was significantly decreased in the Cd group. ASB/Cd combined treatment significantly improves the damage of chicken kidneys by ameliorating Cd-induced kidney ERS and apoptosis. Cd can cause the disorder of the
GRP78 signal axis, activate the PERK-ATF4-CHOP pathway, aggravate the structural damage and dysfunction of ER, and promote the apoptosis of chicken kidneys, while the above changes were significantly alleviated in the ASB/Cd group. The results showed that ASB antagonizes the negative effects of Cd and against Cd-induced apoptosis in chicken kidneys via ERS signaling pathway.