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. 2015:2015:280958.
doi: 10.1155/2015/280958. Epub 2015 Feb 5.

Cinnabar induces renal inflammation and fibrogenesis in rats

Ying Wang  1 , Dapeng Wang  1 , Jie Wu  1 , Bohan Wang  1 , Liangjun Wang  1 , Xin Gao  1 , Hai Huang  1 , Honglin Ma  1
Affiliations

Cinnabar induces renal inflammation and fibrogenesis in rats

Ying Wang et al. Biomed Res Int. 2015.

Abstract

The purpose of this study was to investigate whether cinnabar causes renal inflammation and fibrosis in rats. Rats were dosed orally with cinnabar (1 g/kg/day) for 8 weeks or 12 weeks. The control rats were treated with solvent (5% carboxymethylcellulose solution) over the same time periods, respectively. Renal mercury (RHg), urinary mercury (UHg), serum creatinine (SCr), urine kidney injury molecule 1 (KIM-1), renal pathology, and renal mediators were examined. At both 8 weeks and 12 weeks, RHg, UHg, and urine KIM-1 were significantly higher in the cinnabar group than in the control group, although SCr was unchanged. Kidney lesions in the cinnabar-treated rats occurred mainly in the tubules and interstitium, including vacuolization, protein casts, infiltration of inflammatory cells, and slight increase in interstitial collagen. In addition, mild mesangial proliferation was observed in glomeruli. Moreover, the expression of inflammatory and fibrogenic mediators was upregulated in the cinnabar group. In conclusion, cinnabar may cause kidney damage due to the accumulation of mercury, and renal inflammation and slight fibrogenesis may occur in rats. In the clinic, the potential risk of renal injury due to the prolonged consumption of cinnabar should be considered even though the agent is relatively nontoxic.

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Figures

Figure 1
Figure 1
Cinnabar caused tubulointerstitial damage in rats. Renal sections were stained with hematoxylin and eosin (HE). (a) The control group, 8 weeks. ((b)–(d)) The cinnabar group, 8 weeks. (e) The control group, 12 weeks. ((f)–(h)) The cinnabar group, 12 weeks. (a) and (e) show the normal histology of the kidney. (b) and (f) show vacuolization of tubular cells (indicated by arrows), (c) and (g) show protein casts in tubules (indicated by arrows), and (d) and (h) show infiltration of inflammatory cells in cinnabar-treated rats. Scale bar = 20 μm.
Figure 2
Figure 2
Cinnabar caused mild tubulointerstitial fibrogenesis in rats. Renal sections were stained with Masson. (a) The control group, 8 weeks. (b) The cinnabar group, 8 weeks. (c) The control group, 12 weeks. (d) The cinnabar group, 12 weeks. (e) Bar graph of interstitial collagen (score). Scale bar = 100 μm in ((a)–(d)). ** P < 0.01, compared with the control group (n = 6).
Figure 3
Figure 3
Cinnabar caused glomerular damage in rats. Renal sections were stained with hematoxylin and eosin (HE). (a) Control group, 8 weeks. (b) Cinnabar group, 8 weeks. (c) Control group, 12 weeks. (d) and (e) Cinnabar group, 12 weeks. (b) and (d) show mesangial proliferation. (e) shows focal glomerular sclerosis. Scale bar = 20 μm.
Figure 4
Figure 4
Cinnabar caused mesangial proliferation in rats. Renal sections were stained with periodic acid-Schiff (PAS). (a) Control group, 8 weeks. (b) Cinnabar group, 8 weeks. (c) Control group, 12 weeks. (d) Cinnabar group, 12 weeks. Scale bar = 50 μm.
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