リゾホスファチジン酸(LPA)がSLEモデルマウスの糸球体腎炎を改善させる
Objective: Lupus nephritis is a typical clinical manifestation of SLE. We previously reported that LPA treatment improves depressive-like behavior and microglial activation in MRL/lpr mice (an animal model of SLE). Thus, we examined the effects of LPA on renal function and glomerulonephritis in MRL/...
        Saved in:
      
    
          | Published in | 日本薬理学会年会要旨集 p. 2-B-SS11-1 | 
|---|---|
| Main Authors | , , , , | 
| Format | Journal Article | 
| Language | Japanese | 
| Published | 
            公益社団法人 日本薬理学会
    
        2022
     | 
| Subjects | |
| Online Access | Get full text | 
| ISSN | 2435-4953 | 
| DOI | 10.1254/jpssuppl.96.0_2-B-SS11-1 | 
Cover
| Summary: | Objective: Lupus nephritis is a typical clinical manifestation of SLE. We previously reported that LPA treatment improves depressive-like behavior and microglial activation in MRL/lpr mice (an animal model of SLE). Thus, we examined the effects of LPA on renal function and glomerulonephritis in MRL/lpr mice. Method:18-week-old MRL+/+ mice (n=12) were treated with vehicle and 18-week-old MRL/lpr mice (n=24) were treated with vehicle or LPA (1 mg/kg) for 2 weeks. After the treatment, urine and blood samples were collected, and histological examinations were performed. Results and Discussion: The significant increases in daily urinary albumin levels in MRL/lpr mice were lost by LPA treatment. Creatinine in plasma was not significantly different between the three groups. The significant increases in plasma dsDNA antibody levels in MRL/lpr mice were lost by LPA treatment. The increases of CD68-positive cells in the glomerulus were found in MRL/lpr mice and the increases were suppressed by LPA treatment. The PAS-positive rates in MRL/lpr mice were significantly increased compared to MRL+/+ mice and the increases were significantly suppressed by LPA treatment. These results suggest that LPA treatment improves glomerulonephritis and proteinuria in MRL/lpr mice. | 
|---|---|
| Bibliography: | 96_2-B-SS11-1 | 
| ISSN: | 2435-4953 | 
| DOI: | 10.1254/jpssuppl.96.0_2-B-SS11-1 |