Abstract: TH-PO288
Protective Effects of Brazilian Green Propolis in Sepsis-Induced AKI
Session Information
- AKI Basic: Inflammation and Transcription
November 02, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Acute Kidney Injury
- 001 AKI: Basic
Authors
- Silveira, Marcelo Duarte, University of Sao Paulo School of Medicine, Sao Paulo, Brazil
- Condor Capcha, Jose Manuel, University of Sao Paulo School of Medicine, Sao Paulo, Brazil
- Sanches, Talita R., University of Sao Paulo School of Medicine, Sao Paulo, Brazil
- Moreira, Roberto De Souza, University of Sao Paulo School of Medicine, Sao Paulo, Brazil
- Garnica, Margoth Ramos, University of Sao Paulo School of Medicine, Sao Paulo, Brazil
- Shimizu, Maria HM, University of Sao Paulo School of Medicine, Sao Paulo, Brazil
- Teles de Farias Filho, Flavio, UNCISAL, Maceio,, Alagoas, Brazil
- Andrade, Lucia, University of Sao Paulo School of Medicine, Sao Paulo, Brazil
Background
The pathophysiology of sepsis involves oxidative stress, as well as inflammatory mediator networks, to which NF-κB and TLR4 activation is central. The pharmacological benefits of propolis have been extensively explored, because it might be an important resource for the prevention and treatment of systemic diseases. Brazilian green propolis (BGP) has garnered attention for its promising anti-inflammatory, antioxidant and immunomodulatory properties. We used a cecal ligation and puncture (CLP) model to analyze the role of BGP in sepsis-related organ dysfunction.
Methods
We divided Wistar rats into groups: sham-operated; CLP; and CLP+BGP (500 mg/kg BW ip, 6 h after CLP). Studies were performed at 24 h post-CLP. Data are mean±SD.
Results
Blood GSH was higher in CLP+BGP rats than in CLP rats (0.87±0.4 vs. 0.33±0.1 mg/ml; p<0.001) as was protein expression of MnSOD and eNOS in kidney tissue (138.1±27.4 vs. 100.5±19.7%; p<0.01 and 109.3±14.1 vs. 81.2±26.4%; p<0.05, respectively). In kidney tissue, protein expression of TLR4 and NF-κB was lower in CLP+BGP rats than in CLP rats (111.9±11.9 vs. 164±26.6; p<0.001 and 93.50±7.1 vs. 132±11.3; p<0.001, respectively). Renal expression of CD68 (positive cells/mm2) was lower in CLP+BGP rats than in CLP rats (5.1±1.0 vs. 7.1±2.0; p<0.05). Apoptosis (TUNEL) in kidneys and lungs was lower in CLP+BGP rats than in CLP rats (2.9±2.2 vs. 7.6±3.46 positive cells/0.087 mm2; p<0.05 and 0.04±0.03 vs. 0.08±0.06 positive cells/Total Cells; p<0.001, respectively). BAX protein expression in kidney was lower in CLP+BGP rats than in CLP rats (97±10.9 vs. 135±24.7; p<0.01). BGP also improved kidney mitochondrial morphology (electron microscopy). Myeloperoxidase activity (AU/g) was lower in CLP+BGP rat lungs than in CLP rat lungs (2.32±3.4 vs. 3.62±4.7; p<0.05), as was the number of TLR4-positive cells (0.20±0.07 vs. 0.27±0.10; p<0.001).
Conclusion
In sepsis, BGP protects kidneys and lungs by attenuating oxidative stress and decreasing expression of NF-κB and TLR4. (FAPESP)
Biochemical parameters and NKCC2 protein expression
Clin (ml/min) | UVNa (mEq/day) | UVK (mEq/day) | OSMU mOsm/kg | NKCC2 (%) | |
Sham | 0.82±0.13 | 0.51±0.22 | 0.88±0.17 | 695.4±215.8 | 113.0±23.0 |
CLP | 0.23±0.08 | 1.05±0.51 | 1.47±0.52 | 487.8±204.4 | 47.22±31.0 |
CLP+GP | 0.68±0.36* | 0.64±0.53* | 1.13±0.22* | 873.3±430.7* | 83.0±27.4* |
*p<0.05 vs. CLP
Funding
- Government Support - Non-U.S.