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Calcium Overload and Ros Accumulation Induced by Selenium Deficiency Promote Autophagy in Swine Intestine

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Abstract Background:Selenium deficiency can seriously affect the intestinal status of swine, and cause diarrhea in swine. However, the specific mechanism of selenium intestinal injury caused by selenium deficiency is rarely reported.Methods:Here, to explore the damage of selenium deficiency on the calcium homeostasis and autophagy mechanism of swine, in vivo and in vitro models of swine intestinal selenium deficiency were established. The intestinal model of swine intestine was established by feeding different selenium concentrations. Besides, selenium-deficient medium and normal medium were used to culture IPEC-J2 cells to establish in vitro models. Morphological observation and cell staining were used to determine the way of intestinal injury, and gene expression was quantitatively detected by qPCR and WB.Results:Morphological observations showed that compared with the control group, intestinal cells in the Se-deficiency group were significantly damaged, and autophagosomes increased. MDC staining and cytoplasmic calcium staining results showed that in the Se-deficiency group, autophagy increased and calcium homeostasis was destroyed. Also, according to the ROS test results, the percentage of ROS in the Se-deficiency group is higher than the control group in the in vitro model. Compared with the control group, the protein and mRNA expressions of autophagy and calcium-related genes (Beclin1, LC3-1, LC3-2, ATG5, ATG12, ATG16, mTOR, CAMKK-β, AMPK, SERCA, calpain) in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro. Under the influence of selenium deficiency, the mRNA expression level of selenoproteins decreased significantly, and the steady-state content of some elements was also destroyed. Conclusion:Altogether, our results indicated that selenium deficiency could destroy the calcium homeostasis and antioxidant homeostasis of swine intestine to trigger cell autophagy. Moreover, selenium deficiency reduces the overall expression of selenoproteins and affects the content of elements in the intestine.
Title: Calcium Overload and Ros Accumulation Induced by Selenium Deficiency Promote Autophagy in Swine Intestine
Description:
Abstract Background:Selenium deficiency can seriously affect the intestinal status of swine, and cause diarrhea in swine.
However, the specific mechanism of selenium intestinal injury caused by selenium deficiency is rarely reported.
Methods:Here, to explore the damage of selenium deficiency on the calcium homeostasis and autophagy mechanism of swine, in vivo and in vitro models of swine intestinal selenium deficiency were established.
The intestinal model of swine intestine was established by feeding different selenium concentrations.
Besides, selenium-deficient medium and normal medium were used to culture IPEC-J2 cells to establish in vitro models.
Morphological observation and cell staining were used to determine the way of intestinal injury, and gene expression was quantitatively detected by qPCR and WB.
Results:Morphological observations showed that compared with the control group, intestinal cells in the Se-deficiency group were significantly damaged, and autophagosomes increased.
MDC staining and cytoplasmic calcium staining results showed that in the Se-deficiency group, autophagy increased and calcium homeostasis was destroyed.
Also, according to the ROS test results, the percentage of ROS in the Se-deficiency group is higher than the control group in the in vitro model.
Compared with the control group, the protein and mRNA expressions of autophagy and calcium-related genes (Beclin1, LC3-1, LC3-2, ATG5, ATG12, ATG16, mTOR, CAMKK-β, AMPK, SERCA, calpain) in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro.
Under the influence of selenium deficiency, the mRNA expression level of selenoproteins decreased significantly, and the steady-state content of some elements was also destroyed.
Conclusion:Altogether, our results indicated that selenium deficiency could destroy the calcium homeostasis and antioxidant homeostasis of swine intestine to trigger cell autophagy.
Moreover, selenium deficiency reduces the overall expression of selenoproteins and affects the content of elements in the intestine.

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