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2015 ; 10
(ä): 120
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Paeoniflorin exerts a nephroprotective effect on concanavalin A-induced damage
through inhibition of macrophage infiltration
#MMPMID26204936
Liu C
; Cheng Z
; Wang Y
; Dai X
; Zhang J
; Xue D
Diagn Pathol
2015[Jul]; 10
(ä): 120
PMID26204936
show ga
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
IL1? 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.