Source of Reactive Oxygen Species in Anti-Thy1 Nephritis

Nakamura, Kazuko; Oka, Megumi; Shirai, Masaki; Igarashi, Yoshiharu; Kojima, Kenichiro; Kaneko, Oriyoshi; Hamada, Natsuko; Mera, Junichiro; Masaoka, Hiroyuki; Nagase, Mitsumasa

doi:10.3109/08860229809045127

Cited by 13 publications

(10 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nevertheless, macrophages that infiltrated into the interstitium can release ROS (26). It is reported that ROS generated by the infiltrated macrophages contribute in the development of renal disease (27). Thus, DPPD may have scavenged macrophage-derived ROS and attenuated ROS-mediated fibrogenetic process, a possibility that must be tested in future studies.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Antioxidant on Development of Fibrosis by Cisplatin in Rats

et al. 2009

View full text Add to dashboard Cite

Abstract. Cisplatin causes chronic interstitial disease with fibrosis, but the development mechanism of interstitial fibrosis is not yet understood. We examined the effect of an antioxidant, N,N'-diphenyl-1,4-phenylenediamine (DPPD), on development of interstitial fibrosis induced by cisplatin. Cisplatin increased blood urea nitrogen (BUN), plasma creatinine, and elicited glucosuria and enzymuria at 3 days after administration, but these changes were restored to the normal level after 14 days. Type III collagen increased from 7 days after administration of cisplatin and the expansion of the interstitial fibrosis area became evident at 14 days. Sustained renal fibrosis worsened renal function again at 56 days. Administration of DPPD, which was started at 3 days after cisplatin treatment, significantly inhibited the increase in renal type III collagen contents and the expansion of the interstitial fibrosis area without affecting enzymuria and increased BUN. These results indicate that anti-fibrotic action of DPPD is not secondary due to the inhibition of acute renal injury but is rather a direct effect on renal fibrogenesis. DPPD did not prevent the infiltration of macrophages by cisplatin, suggesting that anti-fibrotic action of DPPD was not mediated by the inhibition of inflammatory cellular influx. It is suggested that reactive oxygen species are involved in cisplatin-induced renal interstitial fibrosis.

show abstract

Section: Discussionmentioning

confidence: 99%

The Effect of Antioxidant on Development of Fibrosis by Cisplatin in Rats

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Reactive oxygen species (ROS) released from inflammatory cells play a critical role in the pathogenesis of thy-1 nephritis [26]. A previous study showed that a scavenger for ROS suppressed urinary protein and the proliferation of mesangial cells in thy-1 nephritis [27].…”

Section: Discussionmentioning

confidence: 99%

Suppressive Mechanisms of Sairei-to on Mesangial Matrix Expansion in Rat Mesangioproliferative Glomerulonephritis

Ono¹,

Liu²,

Makino

et al. 2005

Nephron Exp Nephrol

View full text Add to dashboard Cite

Background: Sairei-to (TJ-114) is a Japanese herbal medicine of standardized quality, originating from traditional Chinese medicine. In the present in vivo study, we investigated the suppressive effects of TJ-114 and related drugs, Shosaiko-to (TJ-9), and Saiboku-to (TJ-96), on mesangioproliferative glomerulonephritis (MsPGN) in rats. TJ-9 is a basal prescription of TJ-96 and TJ-114. We evaluated the efficacy of these drugs on proteinuria, extracellular matrix (ECM) accumulation, and superoxide dismutase (SOD)-activity. Methods: MsPGN in Wistar rats was induced by intravenous injection of rabbit anti-rat thymocyte serum (ATS). TJ-114, TJ-9, TJ-96 (500 mg/kg/day), or prednisolone (PSL, 2 mg/kg/day) was orally administered to the rats as drinking water from the day of ATS injection (day 0) to day 8, when rats were sacrificed and the kidney specimens were collected. Macrophage infiltration was evaluated by immunostaining for ED-1. ECM was measured by trichrome-staining, and fibronectin immunostaining. Northern blotting was performed to clarify the mRNA expression of cytokines and fibronectin. SOD-activity in the homogenate of renal cortex was also evaluated. Results: The amount of urinary protein was significantly decreased only in the TJ-114-treated group compared with the disease control group (p < 0.05). The number of ED-1-positive cells was significantly decreased in all the treatment groups (p < 0.05, respectively). Decreases in the trichrome-stained area were observed moderately in the TJ-114-treated group (66% of control, p < 0.001) and mildly in the PSL-treated group (76% of control, p < 0.001). The staining area of fibronectin in the glomerulus was significantly decreased in all the treated groups except PSL, and was especially suppressed in the TJ-114-treated group (45% of control, p < 0.001). Transforming growth factor (TGF) and connective tissue growth factor (CTGF) expression significantly decreased in the TJ-114-treated group to the control level (p < 0.05). TGF-β, CTGF, and fibronectin mRNA were upregulated in the disease control group, and TJ-114 suppressed these mRNA expressions in glomeruli. The SOD-activity of renal cortex-homogenate was significantly augmented in all the treated groups except PSL, markedly in the TJ-96- and TJ-114-treated groups. Conclusion: These results suggest that TJ-114 ameliorates ECM accumulation in experimental rat MsPGN, partly suppressing TGF-β and CTGF expression through the recovery of SOD-activity.

show abstract

“…Reactive oxygen species (ROS) released from inflammatory cells play a critical role in the pathogenesis of Thy-1 nephritis [24]. A previous study showed that a scavenger for ROS suppressed urinary protein and the proliferation of mesangial cell in Thy-1 nephritis [25].…”

Section: Discussionmentioning

confidence: 99%

Suppressive Effects of Rosmarinic Acid on Mesangioproliferative Glomerulonephritis in Rats

Makino

Ono

Liu

et al. 2002

Nephron

View full text Add to dashboard Cite

Background: Rosmarinic acid is known to be a natural phenolic compound widely distributed in Labiatae herbs such as rosemary, sweet basil, and perilla. In the present study, we evaluated the suppressive effects of rosmarinic acid on mesangioproliferative glomerulonephritis in vivo, which was induced by intravenous injection of rabbit anti-rat thymocyte serum (ATS) to rats. Methods: Rosmarinic acid was orally administered to the rats at a dose of 100 mg/kg/day from the day of ATS injection (day 0) to day 8 when rats were sacrificed. The degree of mesangial cell proliferation and matrix accumulation were evaluated by trichrome staining and by immunostaining for proliferating cell nuclear antigen (PCNA), fibronectin, type IV collagen and fibrin. Superoxide dismutase (SOD)-activity in the homogenate of renal cortex was also evaluated. Results: The number of PCNA-positive cells, staining areas of trichrome, fibronectin, collagen IV and fibrin in the glomerulus were significantly decreased, and SOD-activity of renal cortex homogenate was significantly augmented in rosmarinic acid-treated group. Conclusion: Rosmarinic acid would suppress the proliferation of mesangial cells and glomerular matrix expansion in vivo by its fibrinolytic and anti-oxidative activity.

show abstract

Source of Reactive Oxygen Species in Anti-Thy1 Nephritis

Cited by 13 publications

References 12 publications

The Effect of Antioxidant on Development of Fibrosis by Cisplatin in Rats

The Effect of Antioxidant on Development of Fibrosis by Cisplatin in Rats

Suppressive Mechanisms of Sairei-to on Mesangial Matrix Expansion in Rat Mesangioproliferative Glomerulonephritis

Suppressive Effects of Rosmarinic Acid on Mesangioproliferative Glomerulonephritis in Rats

Contact Info

Product

Resources

About