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Betanin reduces the accumulation and cross-links of collagen in high-fructose-fed rat heart through inhibiting non-enzymatic glycation.
Chem Biol Interact. 2015 Feb 05; 227:37-44.CB

Abstract

We attempted to determine whether betanin (from natural pigments) that has antioxidant properties would be protective against fructose-induced diabetic cardiac fibrosis in Sprague-Dawley rats. Fructose water solution (30%) was accessed freely, and betanin (25 and 100 mg/kg/d) was administered by intra-gastric gavage continuously for 60 d. Rats were sacrificed after overnight fast. The rat blood and left ventricle were collected. In vitro antiglycation assay in bovine serum albumin/fructose system was also performed. In rats treated only with fructose, levels of plasma markers: glucose, insulin, HOMA and glycated hemoglobin rised, left ventricle collagen accumulated and cross-linked, profibrotic factor-transforming growth factor (TGF)-β1 and connective tissue growth factor (CTGF) protein expression increased, and soluble collagen decreased, compared with those in normal rats, showing fructose induces diabetic cardiac fibrosis. Treatment with betanin antagonized the changes of these parameters, demonstrating the antifibrotic role of betanin in the selected diabetic models. In further mechanistic study, betanin decreased protein glycation indicated by the decreased levels of protein glycation reactive intermediate (methylglyoxal), advanced glycation end product (N(ε)-(carboxymethyl) lysine) and receptors for advanced glycation end products (AGEs), antagonized oxidative stress and nuclear factor-κB activation elicited by fructose feeding, suggesting inhibition of glycation, oxidative stress and nuclear factor-κB activation may be involved in the antifibrotic mechanisms. Betanin also showed anitglycative effect in BSA/fructose system, which supported that anitglycation was involved in betanin's protective roles in vivo. Taken together, the potential for using betanin as an auxillary therapy for diabetic cardiomyopathy deserves to be explored further.

Authors+Show Affiliations

College of Life Science and Engineering, Shenyang University, Shenyang 110044, China. Electronic address: hanjunyan@aliyun.com.College of Basic Medical Science, China Medical University, Shenyang 110001, China.College of Life Science and Engineering, Shenyang University, Shenyang 110044, China.College of Life Science and Engineering, Shenyang University, Shenyang 110044, China.College of Food, Shenyang Agricultural University, Shenyang 110866, China. Electronic address: tandehongsy@126.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25559852

Citation

Han, Junyan, et al. "Betanin Reduces the Accumulation and Cross-links of Collagen in High-fructose-fed Rat Heart Through Inhibiting Non-enzymatic Glycation." Chemico-biological Interactions, vol. 227, 2015, pp. 37-44.
Han J, Tan C, Wang Y, et al. Betanin reduces the accumulation and cross-links of collagen in high-fructose-fed rat heart through inhibiting non-enzymatic glycation. Chem Biol Interact. 2015;227:37-44.
Han, J., Tan, C., Wang, Y., Yang, S., & Tan, D. (2015). Betanin reduces the accumulation and cross-links of collagen in high-fructose-fed rat heart through inhibiting non-enzymatic glycation. Chemico-biological Interactions, 227, 37-44. https://doi.org/10.1016/j.cbi.2014.12.032
Han J, et al. Betanin Reduces the Accumulation and Cross-links of Collagen in High-fructose-fed Rat Heart Through Inhibiting Non-enzymatic Glycation. Chem Biol Interact. 2015 Feb 5;227:37-44. PubMed PMID: 25559852.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Betanin reduces the accumulation and cross-links of collagen in high-fructose-fed rat heart through inhibiting non-enzymatic glycation. AU - Han,Junyan, AU - Tan,Chang, AU - Wang,Yiheng, AU - Yang,Shaobin, AU - Tan,Dehong, Y1 - 2015/01/02/ PY - 2014/11/13/received PY - 2014/12/17/revised PY - 2014/12/19/accepted PY - 2015/1/7/entrez PY - 2015/1/7/pubmed PY - 2015/4/15/medline KW - AGEs KW - Diabetic cardiomyopathy KW - Insulin KW - Methylglyoxal KW - NF-κB SP - 37 EP - 44 JF - Chemico-biological interactions JO - Chem Biol Interact VL - 227 N2 - We attempted to determine whether betanin (from natural pigments) that has antioxidant properties would be protective against fructose-induced diabetic cardiac fibrosis in Sprague-Dawley rats. Fructose water solution (30%) was accessed freely, and betanin (25 and 100 mg/kg/d) was administered by intra-gastric gavage continuously for 60 d. Rats were sacrificed after overnight fast. The rat blood and left ventricle were collected. In vitro antiglycation assay in bovine serum albumin/fructose system was also performed. In rats treated only with fructose, levels of plasma markers: glucose, insulin, HOMA and glycated hemoglobin rised, left ventricle collagen accumulated and cross-linked, profibrotic factor-transforming growth factor (TGF)-β1 and connective tissue growth factor (CTGF) protein expression increased, and soluble collagen decreased, compared with those in normal rats, showing fructose induces diabetic cardiac fibrosis. Treatment with betanin antagonized the changes of these parameters, demonstrating the antifibrotic role of betanin in the selected diabetic models. In further mechanistic study, betanin decreased protein glycation indicated by the decreased levels of protein glycation reactive intermediate (methylglyoxal), advanced glycation end product (N(ε)-(carboxymethyl) lysine) and receptors for advanced glycation end products (AGEs), antagonized oxidative stress and nuclear factor-κB activation elicited by fructose feeding, suggesting inhibition of glycation, oxidative stress and nuclear factor-κB activation may be involved in the antifibrotic mechanisms. Betanin also showed anitglycative effect in BSA/fructose system, which supported that anitglycation was involved in betanin's protective roles in vivo. Taken together, the potential for using betanin as an auxillary therapy for diabetic cardiomyopathy deserves to be explored further. SN - 1872-7786 UR - https://www.unboundmedicine.com/medline/citation/25559852/Betanin_reduces_the_accumulation_and_cross_links_of_collagen_in_high_fructose_fed_rat_heart_through_inhibiting_non_enzymatic_glycation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0009-2797(14)00417-7 DB - PRIME DP - Unbound Medicine ER -