Tags

Type your tag names separated by a space and hit enter

Effects of 1, 25-Dihydroxyvitamin D3 on Experimental Autoimmune Myocarditis in Mice.
Cell Physiol Biochem. 2016; 38(6):2219-29.CP

Abstract

BACKGROUND/AIMS

Myocarditis is an important inflammatory disease of the heart which causes life-threatening conditions. 1, 25(OH)2 D3 has effects on multiple systems and diseases. The present study was aimed to investigate the effect of 1, 25(OH)2 D3 on experimental autoimmune myocarditis (EAM), and explored the underlying mechanisms involved.

METHODS

EAM was induced by immunizing BALB/c mice with cardiac α-myosin heavy chain peptides (MyHC-α). 1, 25(OH)2 D3 (1,000 ng/kg once) or vehicle was administered intraperitoneally every other day during the entire experiment. On day 21, transthoracic echocardiography was performed and cardiac inflammatory infiltration was detected by hematoxylin and eosin (HE). The terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) assay, and Western blots for the expression of protein caspase-3 and cleaved-caspase3 were used to evaluate apoptosis. Transmission electron microscopy and Western blots for the expression of protein Beclin-1, LC3B, and P62 were used to evaluate autophagy.

RESULTS

The ratio of heart weight/body weight was significantly reduced in 1, 25(OH)2 D3 -treated EAM mice, compared with vehicle -treated ones. 1, 25(OH)2 D3 treatment improved cardiac function, diminished cell infiltration in cardiac, suppressed myocardial apoptosis, decreased the number of autophagosomes, and decreased the protein expression of Beclin-1, LC3-II and p62.

CONCLUSIONS

The present results demonstrated that administration of 1, 25(OH)2 D3 decreased EAM severity. 1, 25(OH)2 D3 treatment may be a feasible therapeutic approach for EAM.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27184135

Citation

Hu, Fen, et al. "Effects of 1, 25-Dihydroxyvitamin D3 On Experimental Autoimmune Myocarditis in Mice." Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, vol. 38, no. 6, 2016, pp. 2219-29.
Hu F, Yan L, Lu S, et al. Effects of 1, 25-Dihydroxyvitamin D3 on Experimental Autoimmune Myocarditis in Mice. Cell Physiol Biochem. 2016;38(6):2219-29.
Hu, F., Yan, L., Lu, S., Ma, W., Wang, Y., Wei, Y., Yan, X., Zhao, X., Chen, Z., Wang, Z., & Cheng, B. (2016). Effects of 1, 25-Dihydroxyvitamin D3 on Experimental Autoimmune Myocarditis in Mice. Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, 38(6), 2219-29. https://doi.org/10.1159/000445577
Hu F, et al. Effects of 1, 25-Dihydroxyvitamin D3 On Experimental Autoimmune Myocarditis in Mice. Cell Physiol Biochem. 2016;38(6):2219-29. PubMed PMID: 27184135.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of 1, 25-Dihydroxyvitamin D3 on Experimental Autoimmune Myocarditis in Mice. AU - Hu,Fen, AU - Yan,Lianhua, AU - Lu,Shuai, AU - Ma,Wenhan, AU - Wang,Ya, AU - Wei,Yuzhen, AU - Yan,Xiaofei, AU - Zhao,Xin, AU - Chen,Zhijian, AU - Wang,Zhaohui, AU - Cheng,Bo, Y1 - 2016/05/17/ PY - 2016/03/15/accepted PY - 2016/5/18/entrez PY - 2016/5/18/pubmed PY - 2017/2/10/medline SP - 2219 EP - 29 JF - Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology JO - Cell. Physiol. Biochem. VL - 38 IS - 6 N2 - BACKGROUND/AIMS: Myocarditis is an important inflammatory disease of the heart which causes life-threatening conditions. 1, 25(OH)2 D3 has effects on multiple systems and diseases. The present study was aimed to investigate the effect of 1, 25(OH)2 D3 on experimental autoimmune myocarditis (EAM), and explored the underlying mechanisms involved. METHODS: EAM was induced by immunizing BALB/c mice with cardiac α-myosin heavy chain peptides (MyHC-α). 1, 25(OH)2 D3 (1,000 ng/kg once) or vehicle was administered intraperitoneally every other day during the entire experiment. On day 21, transthoracic echocardiography was performed and cardiac inflammatory infiltration was detected by hematoxylin and eosin (HE). The terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) assay, and Western blots for the expression of protein caspase-3 and cleaved-caspase3 were used to evaluate apoptosis. Transmission electron microscopy and Western blots for the expression of protein Beclin-1, LC3B, and P62 were used to evaluate autophagy. RESULTS: The ratio of heart weight/body weight was significantly reduced in 1, 25(OH)2 D3 -treated EAM mice, compared with vehicle -treated ones. 1, 25(OH)2 D3 treatment improved cardiac function, diminished cell infiltration in cardiac, suppressed myocardial apoptosis, decreased the number of autophagosomes, and decreased the protein expression of Beclin-1, LC3-II and p62. CONCLUSIONS: The present results demonstrated that administration of 1, 25(OH)2 D3 decreased EAM severity. 1, 25(OH)2 D3 treatment may be a feasible therapeutic approach for EAM. SN - 1421-9778 UR - https://www.unboundmedicine.com/medline/citation/27184135/Effects_of_1_25_Dihydroxyvitamin_D3_on_Experimental_Autoimmune_Myocarditis_in_Mice_ L2 - https://www.karger.com?DOI=10.1159/000445577 DB - PRIME DP - Unbound Medicine ER -