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Paeoniflorin exerts a nephroprotective effect on concanavalin A-induced damage through inhibition of macrophage infiltration.

Liu C, Cheng Z, Wang Y, Dai X, Zhang J, Xue D - Diagn Pathol (2015)

Bottom Line: PF administration significantly reduced the elevated serum levels of alanine transaminase (ALT), blood urea nitrogen (BUN), creatinine (Cr) and the severity of liver and renal damage compared with that in the conA-vehicle group.Furthermore, immunohistochemical analysis showed that macrophages secreted CXCR3 in the kidneys of the conA-vehicle mice.PF administration attenuated conA-induced renal damage, at least in part, by inhibiting the over-activated CXCR3/CXCL11 signal axis.

View Article: PubMed Central - PubMed

Affiliation: Experimental Research Center, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, China. liucheng0082010@163.com.

ABSTRACT

Background: It is well established that macrophage infiltration is involved in concanavalin A (conA)-induced liver injury. However, the role of macrophages in conA-induced renal injury remains unknown. The aims of this study were to investigate macrophage infiltration in conA-induced renal injury and determine whether paeoniflorin (PF) could inhibit macrophage infiltration into the kidney.

Methods: BALB/C mice were pre-treated with or without PF 2 h (h) before conA injection. At 8 h after con A injection, all the mice were sacrificed; The liver and kidney histology were studied. The renal CD68 expression was detected by immunohistochemical and real-time PCR analysis. The level of expression of C-X-C chemokine receptor type 3 (CXCR3) was analyzed by western blot, immunohistochemical and real-time PCR. The pathophysiological involvement of CXCR3 in macrophage infiltration were investigated using dual-colour immunofluorescence microscopy.

Results: PF administration significantly reduced the elevated serum levels of alanine transaminase (ALT), blood urea nitrogen (BUN), creatinine (Cr) and the severity of liver and renal damage compared with that in the conA-vehicle group. PF administration inhibited the increase in renal IL1β mRNA expression and concentration. Furthermore, immunohistochemical analysis showed that macrophages secreted CXCR3 in the kidneys of the conA-vehicle mice. Immunofluorescence microscopy demonstrated CXCR3 bound tightly to C-X-C motif ligand 11 (CXCL11) in the kidneys of the conA-vehicle mice and showed that PF treatment could suppress CXCR3/CXCL11 over-activation.

Conclusions: Macrophage infiltration was a notable pathological change in the kidneys of conA-treated mice. PF administration attenuated conA-induced renal damage, at least in part, by inhibiting the over-activated CXCR3/CXCL11 signal axis.

No MeSH data available.


Related in: MedlinePlus

Effect of PF on CXCR3 and CXCL11 expression in conA-induced renal injury. a CXCR3 immunohistochemical staining (×400, n = 3). b CXCR3 mRNA expression was detected using real-time PCR (n = 6), c CXCL11 mRNA expression was detected using real-time PCR (n = 6), d CXCR3 and CXCL11 were detected by western-blot (n = 4). PF (30 mg/kg) was administered orally 2 h before injection of conA or vehicle for 8 h
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Fig5: Effect of PF on CXCR3 and CXCL11 expression in conA-induced renal injury. a CXCR3 immunohistochemical staining (×400, n = 3). b CXCR3 mRNA expression was detected using real-time PCR (n = 6), c CXCL11 mRNA expression was detected using real-time PCR (n = 6), d CXCR3 and CXCL11 were detected by western-blot (n = 4). PF (30 mg/kg) was administered orally 2 h before injection of conA or vehicle for 8 h

Mentions: Chemokines play an important role in macrophage accumulation at the inflammatory site. CXCR3 and its ligands have been suggested to be one of the most important chemokine axes that promote the arrival of cells into the injured tissues [11]. As shown in Fig. 5a, CXCR3 was weakly stained in non-conA mouse kidneys. In conA-vehicle mouse kidneys, CXCR3 increased significantly and was largely expressed in the renal interstitium, and not in the tubular epithelial cells. In conA-PF mouse kidneys, CXCR3 was suppressed compared with the conA-vehicle group; this was also confirmed by real-time PCR (Fig. 5b).Fig. 5


Paeoniflorin exerts a nephroprotective effect on concanavalin A-induced damage through inhibition of macrophage infiltration.

Liu C, Cheng Z, Wang Y, Dai X, Zhang J, Xue D - Diagn Pathol (2015)

Effect of PF on CXCR3 and CXCL11 expression in conA-induced renal injury. a CXCR3 immunohistochemical staining (×400, n = 3). b CXCR3 mRNA expression was detected using real-time PCR (n = 6), c CXCL11 mRNA expression was detected using real-time PCR (n = 6), d CXCR3 and CXCL11 were detected by western-blot (n = 4). PF (30 mg/kg) was administered orally 2 h before injection of conA or vehicle for 8 h
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4513624&req=5

Fig5: Effect of PF on CXCR3 and CXCL11 expression in conA-induced renal injury. a CXCR3 immunohistochemical staining (×400, n = 3). b CXCR3 mRNA expression was detected using real-time PCR (n = 6), c CXCL11 mRNA expression was detected using real-time PCR (n = 6), d CXCR3 and CXCL11 were detected by western-blot (n = 4). PF (30 mg/kg) was administered orally 2 h before injection of conA or vehicle for 8 h
Mentions: Chemokines play an important role in macrophage accumulation at the inflammatory site. CXCR3 and its ligands have been suggested to be one of the most important chemokine axes that promote the arrival of cells into the injured tissues [11]. As shown in Fig. 5a, CXCR3 was weakly stained in non-conA mouse kidneys. In conA-vehicle mouse kidneys, CXCR3 increased significantly and was largely expressed in the renal interstitium, and not in the tubular epithelial cells. In conA-PF mouse kidneys, CXCR3 was suppressed compared with the conA-vehicle group; this was also confirmed by real-time PCR (Fig. 5b).Fig. 5

Bottom Line: PF administration significantly reduced the elevated serum levels of alanine transaminase (ALT), blood urea nitrogen (BUN), creatinine (Cr) and the severity of liver and renal damage compared with that in the conA-vehicle group.Furthermore, immunohistochemical analysis showed that macrophages secreted CXCR3 in the kidneys of the conA-vehicle mice.PF administration attenuated conA-induced renal damage, at least in part, by inhibiting the over-activated CXCR3/CXCL11 signal axis.

View Article: PubMed Central - PubMed

Affiliation: Experimental Research Center, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, China. liucheng0082010@163.com.

ABSTRACT

Background: It is well established that macrophage infiltration is involved in concanavalin A (conA)-induced liver injury. However, the role of macrophages in conA-induced renal injury remains unknown. The aims of this study were to investigate macrophage infiltration in conA-induced renal injury and determine whether paeoniflorin (PF) could inhibit macrophage infiltration into the kidney.

Methods: BALB/C mice were pre-treated with or without PF 2 h (h) before conA injection. At 8 h after con A injection, all the mice were sacrificed; The liver and kidney histology were studied. The renal CD68 expression was detected by immunohistochemical and real-time PCR analysis. The level of expression of C-X-C chemokine receptor type 3 (CXCR3) was analyzed by western blot, immunohistochemical and real-time PCR. The pathophysiological involvement of CXCR3 in macrophage infiltration were investigated using dual-colour immunofluorescence microscopy.

Results: PF administration significantly reduced the elevated serum levels of alanine transaminase (ALT), blood urea nitrogen (BUN), creatinine (Cr) and the severity of liver and renal damage compared with that in the conA-vehicle group. PF administration inhibited the increase in renal IL1β mRNA expression and concentration. Furthermore, immunohistochemical analysis showed that macrophages secreted CXCR3 in the kidneys of the conA-vehicle mice. Immunofluorescence microscopy demonstrated CXCR3 bound tightly to C-X-C motif ligand 11 (CXCL11) in the kidneys of the conA-vehicle mice and showed that PF treatment could suppress CXCR3/CXCL11 over-activation.

Conclusions: Macrophage infiltration was a notable pathological change in the kidneys of conA-treated mice. PF administration attenuated conA-induced renal damage, at least in part, by inhibiting the over-activated CXCR3/CXCL11 signal axis.

No MeSH data available.


Related in: MedlinePlus