TY - JOUR
T1 - Beneficial effect of Azadirachta indica on advanced glycation end-product in streptozotocin-diabetic rat
AU - Perez Gutierrez, Rosa Martha
AU - De Jesus Martinez Ortiz, Maria
N1 - Publisher Copyright:
© 2014 Informa Healthcare USA, Inc. All rights reserved.
PY - 2014/11/1
Y1 - 2014/11/1
N2 - Context: Both oxidation and hyperglycemia cause increased glycation and the formation of advanced glycation end-products (AGEs) which underlie the complications of diabetes.Objective: The goal of this article is to determine the effect of the chloroform extract from leaves of Azadirachta indica A. Juss; (Meliaceae) (AI) on the formation of glycated protein.Materials and methods: Chloroform extract was subjected to in vitro bioassays to evaluate advanced glycation end-products formation. Bovine serum albumin (BSA)-glucose, BSA-methylglyoxal, Amadori-rich protein, glycated hemoglobin, oxidation, and glycation of LDL were determined. Doses of AI of 200mg/kg/d by oral gavage were administered once daily for 30d, at streptozotocin-induced diabetic rats. After this period, renal damage (TBARS), glucose, methylglyoxal, glycolaldehyde, and tail tendon collagen were investigated.Results and discussion: AI exhibits protective action in BSA against glycation formation, GHb, protein levels, and LDL against glycation and oxidation. The renal glucose level decreases a 3.9mg/g wet tissue. TBA-reactive substance showed a significant decrease to 1.82mmol/mg protein. In addition, AI showed inhibitory activity against AGEs formation, methylglyoxal, and glycolaldehyde levels in kidney. Treatment with AI in rat tail tendon produced a reduction in cross-linking of collagen proteins. The antiglycation activities of A. indica were attributed in part to their antioxidant activity. AI alleviated oxidative stress under diabetic conditions through the inhibition of lipid peroxidation prevents the onset renal damage.Conclusion: We found that A. indica is an inhibitor AGE formation, and oxidative stress with a renoprotective effect, which are considered to play important roles in diabetic kidney disease.
AB - Context: Both oxidation and hyperglycemia cause increased glycation and the formation of advanced glycation end-products (AGEs) which underlie the complications of diabetes.Objective: The goal of this article is to determine the effect of the chloroform extract from leaves of Azadirachta indica A. Juss; (Meliaceae) (AI) on the formation of glycated protein.Materials and methods: Chloroform extract was subjected to in vitro bioassays to evaluate advanced glycation end-products formation. Bovine serum albumin (BSA)-glucose, BSA-methylglyoxal, Amadori-rich protein, glycated hemoglobin, oxidation, and glycation of LDL were determined. Doses of AI of 200mg/kg/d by oral gavage were administered once daily for 30d, at streptozotocin-induced diabetic rats. After this period, renal damage (TBARS), glucose, methylglyoxal, glycolaldehyde, and tail tendon collagen were investigated.Results and discussion: AI exhibits protective action in BSA against glycation formation, GHb, protein levels, and LDL against glycation and oxidation. The renal glucose level decreases a 3.9mg/g wet tissue. TBA-reactive substance showed a significant decrease to 1.82mmol/mg protein. In addition, AI showed inhibitory activity against AGEs formation, methylglyoxal, and glycolaldehyde levels in kidney. Treatment with AI in rat tail tendon produced a reduction in cross-linking of collagen proteins. The antiglycation activities of A. indica were attributed in part to their antioxidant activity. AI alleviated oxidative stress under diabetic conditions through the inhibition of lipid peroxidation prevents the onset renal damage.Conclusion: We found that A. indica is an inhibitor AGE formation, and oxidative stress with a renoprotective effect, which are considered to play important roles in diabetic kidney disease.
KW - Advanced glycation end-products formation
KW - Diabetic kidney disease
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=84912122632&partnerID=8YFLogxK
U2 - 10.3109/13880209.2014.895389
DO - 10.3109/13880209.2014.895389
M3 - Artículo
SN - 1388-0209
VL - 52
SP - 1435
EP - 1444
JO - Pharmaceutical Biology
JF - Pharmaceutical Biology
IS - 11
ER -