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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Inflamm+Res
2017 ; 10
(ä): 135-142
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An in vitro model of renal inflammation after ischemic oxidative stress injury:
nephroprotective effects of a hyaluronan ester with butyric acid on mesangial
cells
#MMPMID28932127
Baraldi O
; Bianchi F
; Menghi V
; Angeletti A
; Croci Chiocchini AL
; Cappuccilli M
; Aiello V
; Comai G
; La Manna G
J Inflamm Res
2017[]; 10
(ä): 135-142
PMID28932127
show ga
BACKGROUND: Acute kidney injury, known as a major trigger for organ fibrosis and
independent predictor of chronic kidney disease, is characterized by mesangial
cell proliferation, inflammation and unbalance between biosynthesis and
degradation of extracellular matrix. Therapeutic approaches targeting the
inhibition of mesangial cell proliferation and matrix expansion may represent a
promising opportunity for the treatment of kidney injury. An ester of hyaluronic
acid and butyric acid (HB) has shown vasculogenic and regenerative properties in
renal ischemic-damaged tissues, resulting in enhanced function recovery and minor
degree of inflammation in vivo. This study evaluated the effect of HB treatment
in mesangial cell cultures exposed to H(2)O(2)-induced oxidative stress.
MATERIALS AND METHODS: Lactate dehydrogenase release and caspase-3 activation
were measured using mesangial cells prepared from rat kidneys to assess necrosis
and apoptosis. Akt and p38 phosphorylation was analyzed to identify the possible
mechanism underlying cell response to HB treatment. The relative expressions of
matrix metallopeptidase 9 (MPP-9) and collagen type 1 alpha genes were also
analyzed by quantitative real-time polymerase chain reaction. Cell proliferation
rate and viability were measured using thiazolyl blue assay and flow cytometry
analysis of cell cycle with propidium iodide. RESULTS: HB treatment promoted
apoptosis of mesangial cells after H(2)O(2)-induced damage, decreased cellular
proliferation and activated p38 pathway, increasing expression of its target gene
MPP-9. CONCLUSION: This in vitro model shows that HB treatment seems to redirect
mesangial cells toward apoptosis after oxidative damage and to reduce cell
proliferation through p38 MAPK pathway activation and upregulation of MPP-9 gene
expression involved in mesangial matrix remodeling.