Abstract
High-concentrate feeding can induce subacute ruminal acidosis, which leads to mammary tissue injury in dairy cows. Therefore, the purpose of this research was to evaluate the effect of high-concentrate feeding on STIM1 (stromal interaction molecule 1)/ORAI1 (Orai calcium release-activated calcium modulator 1)-mediated inflammation, endoplasmic reticulum stress (ERS), and apoptosis in the mammary tissue of dairy cows. A total of 12 healthy mid-lactating Holstein cows of similar weight were randomly allotted into the following 2 groups: a high-concentrate (HC) group (concentrate:forage = 6:4) and a low-concentrate (LC) group (concentrate:forage = 4:6). The trial lasted for 3 wk. After the feeding experiment, rumen fluid, lacteal vein blood, and mammary tissue samples were collected. The results showed that the HC diet significantly increased blood lipopolysaccharide levels, decreased ruminal pH, and upregulated the concentrations of Ca2+ and proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, and the enzyme activities of caspase-3, caspase-9, PKC, and IKK. The upregulation of STIM1, ORAI1, PKCα, IKKβ, phosphorylated-IκBα, phosphorylated-p65, TNF-α, and IL-1α proteins in the HC group indicated activation of the STIM1/ORAI1-mediated inflammatory signaling pathway compared with that in the LC group. The HC diet also induced ERS by increasing the mRNA and protein abundances of GRP78, CHOP, PERK, ATF6, and IRE1α in the mammary tissue. Compared with the LC group, the mRNA expression levels and protein abundances of caspase-3, cleaved caspase-3, caspase-9, and BAX were markedly increased in the HC group. However, the mRNA and protein expression levels of Bcl-2 were significantly decreased in the HC group. Therefore, this study demonstrated that the HC diet can activate the store-operated calcium entry channel by upregulating the expression of STIM1 and ORAI1 and induce inflammation, ERS, and apoptosis in the mammary tissue of dairy cows.
Highlights
To improve production performance and economic returns, dairy cows are often fed large amounts of concentrate feeds, which are rich in fermentable carbohydrates
Under SARA conditions, a large amount of LPS is released by gramnegative bacteria in the rumen, which passes through the epithelial barrier of the digestive tract, transfers to the circulatory system, and migrates to the mammary tissue, where it causes an inflammatory reaction in mammary tissue and produces a large number of cytokines and acute phase proteins (Gozho et al, 2007)
These results showed that SARA activated the store-operated calcium entry (SOCE) channel by upregulating the expression of the STIM1 and ORAI1 genes and proteins, thereby leading to calcium influx
Summary
To improve production performance and economic returns, dairy cows are often fed large amounts of concentrate feeds, which are rich in fermentable carbohydrates. Concentrated feed can greatly improve cows’ milk yield, it affects their health at the same time. These concentrated feeds are high in starch and energy and low in fiber, and too much concentrate intake in ruminants leads to the accumulation of VFA in the rumen and a decrease in ruminal pH, which can cause SARA (Penner et al, 2010). Long-term exposure to SARA reduces the feed intake of dairy cows and increases the risk of laminitis, liver abscess, and inflammatory reactions. It seriously endangers the health of dairy cows and reduces milk yield and quality, thereby causing substantial economic losses to the dairy industry (Chang et al, 2015a). Under SARA conditions, a large amount of LPS is released by gramnegative bacteria in the rumen, which passes through the epithelial barrier of the digestive tract, transfers to the circulatory system, and migrates to the mammary tissue, where it causes an inflammatory reaction in mammary tissue and produces a large number of cytokines and acute phase proteins (Gozho et al, 2007)
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