Crocin Protects Podocytes Against Oxidative Stress and Inflammation Induced by High Glucose Through Inhibition of NF-κB

Autor: Jie Lei, Xiaoxia Liu, Puxun Tian, Sutong Li, Junle Yang, Yi Gao
Jazyk: angličtina
Rok vydání: 2017
Předmět:
0301 basic medicine
Pyrrolidines
Physiology
Diabetic nephropathy
medicine.disease_cause
Antioxidants
NF-κB
lcsh:Physiology
Podocyte
Crocin
chemistry.chemical_compound
Mice
0302 clinical medicine
Pyrrolidine dithiocarbamate
NF-KappaB Inhibitor alpha
lcsh:QD415-436
Cell Line
Transformed

biology
lcsh:QP1-981
Podocytes
Microfilament Proteins
Intracellular Signaling Peptides and Proteins
NF-kappa B
Drug Synergism
Drug Combinations
medicine.anatomical_structure
030220 oncology & carcinogenesis
Signal Transduction
medicine.medical_specialty
Nephrin
lcsh:Biochemistry
03 medical and health sciences
Thiocarbamates
Internal medicine
medicine
Animals
WT1 Proteins
Adaptor Proteins
Signal Transducing

Membrane Proteins
medicine.disease
Carotenoids
Cytoskeletal Proteins
Oxidative Stress
030104 developmental biology
Endocrinology
Glucose
chemistry
Gene Expression Regulation
biology.protein
Podocin
Synaptopodin
Oxidative stress
Zdroj: Cellular Physiology and Biochemistry, Vol 42, Iss 4, Pp 1481-1492 (2017)
ISSN: 1421-9778
1015-8987
Popis: Background/Aims: Diabetic nephropathy (DN) is a microangiopathic disease characterized by excessive urinary albumin excretion, which occurs in 30% of patients with diabetes mellitus. It is the second leading cause of end-stage renal diseases in China. Nuclear factor-kappa B (NF-κB) is reported to be closely correlated with the inflammation underlying diabetes-associated renal damage. Crocin, a plant-derived compound, has antioxidant properties that may inhibit NF-κB. Methods: In the present study, we used a conditionally immortalized mouse podocyte cell line to explore whether crocin could effectively block albuminuria. Cells were incubated with 15 or 25 mM D-glucose to mimic diabetic conditions. The expression of Wilms tumor 1 (WT-1) and synaptopodin was evaluated to identify differentiated podocytes, and the expression of nephrin, podocin, and CD2ap was measured as markers of slit diaphragms, the main structures within the glomerular filtration barrier. Results: The high-glucose conditions led to reduced nephrin, podocin, and CD2ap expression, which was prevented by pretreatment with crocin. The oxidative stress and pro-inflammatory response of podocytes associated with DN induced by high glucose were also reduced by crocin pretreatment. Phosphorylated IκBα (p-IκBα) expression induced by high glucose was also significantly decreased by crocin pretreatment. Moreover, pyrrolidine dithiocarbamate, a NF-κB inhibitor, pyrrolidine dithio carbamate, augmented the protective effects of crocin. Conclusion: Our results demonstrate a protective role of crocin against damage to podocytes and slit diaphragms under high-glucose conditions via inhibition of NF-κB. This study presents a potential therapy for DN and contributes to the understanding of the mechanism underlying DN.
Databáze: OpenAIRE