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Role of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) and renal hemodynamics on obesity related renal damage
| Content Provider | Semantic Scholar |
|---|---|
| Author | Maheshwari, Mani |
| Copyright Year | 2018 |
| Abstract | Obesity is a public health problem associated with salt sensitive hypertension, kidney inflammation, and fibrosis. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a tetra peptide with anti-inflammatory and anti-fibrotic properties; however, its effect on preventing kidney damage in obesity is unknown. We hypothesized that Zucker obese (ZO) rats on a high-salt (HS) diet develop renal damage, inflammation, and fibrosis and this is prevented with Ac-SDKP treatment. Zucker Lean (ZL) and ZO rats (8 weeks old) were treated with Ac-SDKP (1.6 mg/kg/day) while maintained on either a normal-salt (NS; 0.4%) or HS (4%) diet for 8 weeks. Systolic blood pressure (SBP), albuminuria, renal inflammation, and fibrosis were evaluated. HS diet increased macrophage infiltration in the kidneys of both ZL and ZO rats but was significantly higher in ZO rats receiving the HS diet (ZL+NS, 13.9±1.3 vs ZL+HS, 19.14±1.5 and ZO+NS, 25.5±1.4 vs ZO+HS, 87.8 ± 10.8 cells/mm; P <0.05). Ac-SDKP prevented macrophage infiltration in ZO rats (ZO+HS+Ac-SDKP, 32.18±2.4 cells/mm P <0.05). Similarly, glomerulosclerosis, cortical and medullary interstitial fibrosis were increased in ZO rats fed the HS diet, and Ac-SDKP attenuated these alterations (P <0.05). SBP was increased in ZO rats fed the HS diet (ZO+NS, 121.3±8.9 vs ZO+HS, 164±6.9 mmHg; P <0.05), and significantly decreased with Ac-SDKP treatment (P =0.004). Albuminuria was higher in ZO rats than in ZL rats; however, neither HS nor Ac-SDKP treatment affected it. We concluded that AcSDKP treatment in ZO rats fed a HS diet prevented renal damage by reducing inflammation, fibrosis, and BP. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://mds.marshall.edu/cgi/viewcontent.cgi?article=2197&context=etd |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |