title: Protective effects of naringenin in cardiorenal syndrome.
abstract: Cardiorenal syndrome is a complicated and bidirectional interrelationship between the heart and kidneys. Naringenin (NG) is a naturally occurring flavonoid possessing various biological and pharmacological properties.
  
  
  
  We tested whether NG could improve cardiac and renal function in a rat model of cardiorenal syndrome.
  
  
  
  The results showed that NG-attenuated cardiac remodeling and cardiac dysfunction in rats with cardiorenal syndrome, as evidenced by decrease of left ventricle weight (LVW), increase of body weight (BW), decrease of LVW/BW, decrease of concentrations of serum creatinine, blood urea nitrogen, type-B natriuretic peptide, aldosterone, angiotensin (Ang) II, C-reactive protein, and urine protein, increase of left ventricular systolic pressure and falling rates of left ventricular pressure (dp/dtmax), and decrease of left ventricular diastolic pressure, left ventricular end-diastolic pressure, and -dp/dtmax. NG significantly inhibited the increase of lipid profiles including low-density lipoprotein, TC, and TG in rats. In addition, NG significantly inhibited the increase of cardiac expression of IL-1β, IL-6, and interferon γ. Moreover, NG decreased malonaldehyde level, increased superoxide dismutase activity and glutathione content in rats, and increased the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and catalytic subunit of γ-glutamylcysteine ligase (GCLc) in rats and Ang II-treated cardiac fibroblasts. Inhibition of Nrf2 and glutathione synthesis significantly suppressed NG-induced decrease of ROS level. Inhibition of Nrf2 markedly suppressed NG-induced increase of GCLc expression in Ang II-treated cardiac fibroblasts.
  
  
  
  The data provide novel options for therapy of patients and new insights into the cardioprotective effects of NG in cardiorenal syndrome.
authors.affiliation: Department of Nephrology, Yanan University Affiliated Hospital, Yan'an, Shaanxi, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Nephrology, Yan'an People's Hospital, Yan'an, Shaanxi, China.
authors.forename: Wenjun
authors.initials: W
authors.lastname: An
authors.affiliation: Department of Cardiovascular Internal Medicine, Yan'an People's Hospital, Yan'an, Shaanxi, China. Electronic address: aibao_gao111@126.com.
authors.forename: Aibao
authors.initials: A
authors.lastname: Gao
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D015415:Biomarkers / Q000378:metabolism; D059347:Cardio-Renal Syndrome / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D044950:Flavanones / Q000494:pharmacology / Q000627:therapeutic use*; D006352:Heart Ventricles / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D016896:Treatment Outcome
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D044950:Flavanones; C005273:naringenin
keywords: Cardiorenal syndrome; GCLc; Naringenin; Nrf2; Oxidative stress