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. 2015:2015:867140.
doi: 10.1155/2015/867140. Epub 2015 Dec 29.

Tanshinone IIA Attenuates Renal Fibrosis after Acute Kidney Injury in a Mouse Model through Inhibition of Fibrocytes Recruitment

Chunming Jiang  1 , Qiuyuan Shao  1 , Bo Jin  1 , Rujun Gong  2 , Miao Zhang  1 , Biao Xu  3
Affiliations

Tanshinone IIA Attenuates Renal Fibrosis after Acute Kidney Injury in a Mouse Model through Inhibition of Fibrocytes Recruitment

Chunming Jiang et al. Biomed Res Int. 2015.

Abstract

Acute kidney injury (AKI) is associated with an increased risk of developing advanced chronic kidney disease (CKD) VSports手机版. Yet, effective interventions to prevent this conversion are unavailable for clinical practice. In this study, we examined the beneficial effects of Tanshinone IIA on renal fibrosis in a mouse model of folic acid induced AKI. We found that Tanshinone IIA treatment significantly attenuated the folic acid elicited kidney dysfunction on days 3, 14, and 28. This effect was concomitant with a much lessened accumulation of fibronectin and collagen in tubulointerstitium 28 days after folic acid injury, denoting an ameliorated renal fibrosis. The kidney protective and antifibrotic effect of Tanshinone IIA was likely attributable to an early inhibition of renal recruitment of fibrocytes positive for both CD45 and collagen I. Mechanistically, Tanshinone IIA treatment not only markedly diminished renal expression of chemoattractants for fibrocytes such as TGFβ1 and MCP-1, but also significantly reduced circulating fibrocytes at the acute phase of kidney injury. These data suggested that Tanshinone IIA might be a novel therapy for preventing progression of CKD after AKI. .

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Figure 1
Figure 1
Tanshinone IIA ameliorates renal dysfunction in mice with folic acid induced acute kidney injury. Graphs show the time course of BUN and serum creatinine levels at day 3 (a, d), day 14 (b, e), and day 28 (c, f) among different groups (n = 9). Data are expressed as the mean ± SEM. ★ P < 0.01 versus group TS; ★★ P < 0.01 versus group FA. Notes: blood urea nitrogen (BUN). Ctrl: mice treated with vehicle alone; TS: mice treated with Tanshinone IIA alone; FA: folic acid-treated mice followed by vehicle treatment; FA + TS: folic acid-treated mice subjected to Tanshinone IIA injection for 3 consecutive days.
Figure 2
Figure 2
Tanshinone IIA reduces collagen deposition in the kidney 28 days after folic acid injury. (a) Representative Masson-stained sections of renal cortices at day 28 (original magnification ×200). (b) Semiquantification of kidney fibrosis score from Masson-stained sections. (c) Total kidney collagen content determined by hydroxyproline detection among different groups (n = 6). Data are expressed as the mean ± SEM (n = 6 or 9). ★ P < 0.01 versus group TS; ★★ P < 0.01 versus group FA. Notes: Ctrl: mice treated with vehicle alone; TS: mice treated with Tanshinone IIA alone; FA: folic acid-treated mice followed by vehicle treatment; FA + TS: folic acid-treated mice subjected to Tanshinone IIA injection for 3 consecutive days.
Figure 3
Figure 3
Tanshinone IIA inhibits fibronectin expression in the kidney 28 days after folic acid injury. (a) Representative images of fibronectin expression at day 28 stained by immunofluorescence (original magnification ×100). (b) Semiquantification of kidney fibronectin deposition from (a). (c) Representative immunoblots and semiquantification (d) of fibronectin in kidney cortical tissue lysates at day 28. Data are expressed as the mean ± SEM (n = 9). ★ P < 0.01 versus group TS; ★★ P < 0.01 versus group FA. Notes: Ctrl: mice treated with vehicle alone; TS: mice treated with Tanshinone IIA alone; FA: folic acid-treated mice followed by vehicle treatment; FA + TS: folic acid-treated mice subjected to Tanshinone IIA injection for 3 consecutive days.
Figure 4
Figure 4
Tanshinone IIA inhibits recruitment of fibrocytes into the folic acid-injured kidney. (a) Representative images of fibrocytes in the kidney (yellow arrows), determined by dual staining of CD45 (green color) and collagen I (red color) in the kidney. (b) Quantification of fibrocytes in kidney sections evaluated in five random fields per section and five sections per kidney. Data are expressed as the mean ± SEM (n = 9). ★ P < 0.01 versus group TS; ★★ P < 0.01 versus group FA. Notes: Ctrl: mice treated with vehicle alone; TS: mice treated with Tanshinone IIA alone; FA: folic acid-treated mice followed by vehicle treatment; FA + TS: folic acid-treated mice subjected to Tanshinone IIA injection for 3 consecutive days.
Figure 5
Figure 5
Tanshinone IIA inhibits TGF-β1 expression in folic acid-injured kidney at day 3. (a) Representative images and semiquantification (b) of TGF-β1 (original magnification ×400) stained by immunohistochemistry in the kidney sections at day 3. (c) Representative immunoblot and quantification (d) of TGF-β1 in kidney cortical tissue lysates at day 3. Data are expressed as the mean ± SEM (n = 9). ★ P < 0.01 versus group TS; ★★ P < 0.01 versus group FA. Notes: transforming growth factor-beta 1 (TGF-β1); Ctrl: mice treated with vehicle alone; TS: mice treated with Tanshinone IIA alone; FA: folic acid-treated mice followed by vehicle treatment; FA + TS: folic acid-treated mice subjected to Tanshinone IIA injection for 3 consecutive days.
Figure 6
Figure 6
Tanshinone IIA inhibits MCP-1 expression in the folic acid-injured kidney at day 3. (a) Representative images and semiquantification (b) of MCP-1 (original magnification ×100) stained by immunohistochemistry in the kidney sections at day 3. (c) Representative immunoblot and quantification (d) of MCP-1 in kidney cortical tissue lysates at day 3. Data are expressed as the mean ± SEM (n = 9). ★ P < 0.01 versus group TS; ★★ P < 0.01 versus group FA. Notes: monocyte chemotactic protein 1 (MCP-1); Ctrl: mice treated with vehicle alone; TS: mice treated with Tanshinone IIA alone; FA: folic acid-treated mice followed by vehicle treatment; FA + TS: folic acid-treated mice subjected to Tanshinone IIA injection for 3 consecutive days.
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