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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 Am+J+Transl+Res
2018 ; 10
(2
): 402-410
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Augmenter of liver regeneration (ALR) regulates acute pancreatitis via inhibiting
HMGB1/TLR4/NF-?B signaling pathway
#MMPMID29511434
Pan LF
; Yu L
; Wang LM
; He JT
; Sun JL
; Wang XB
; Wang H
; Bai ZH
; Feng H
; Pei HH
Am J Transl Res
2018[]; 10
(2
): 402-410
PMID29511434
show ga
This research aimed to explore the effect of augmenter of liver regeneration
(ALR) in acute pancreatitis (AP) of mice and the underlying mechanism. Caerulein
were given to mice to get AP models. AP mice were given saline, ALR plasmids or
negative control plasmids. Then, pancreas tissues were fixed and stained for
histological examination. The levels of serum amylase, serum lipase, MPO, HMGB1,
TNF-?, IL-1? as well as MCP-1 were detected by ELISA assay. The mRNA levels of
TLR4, p65, I?B?, iNOS, COX-2 and GAPDH were examined by RT-qPCR. The protein
levels of HMGB1, TLR4, MD2, MyD88, I?B? and GAPDH were detected by western
blotting. ALR decreased serum amylase as well as lipase levels and alleviated the
histopathological alterations of the pancreas in AP mice. ALR decreased the MPO
activity of pancreas in AP Mice. ALR decreased the HMGB1/TLR4 signaling pathway
in AP Mice. ALR decreased pancreas IL-1? and MCP-1 in AP mice, and also decreased
plasma TNF-? and IL-1? in AP mice. ALR attenuated the cerulein-caused increase in
p65 mRNA and protein levels, but had no effects on mRNA and protein levels of
I?B?. The AP mice significantly promoted the mRNA levels of iNOS and COX-2 that
was inhibited by ALR. HNE formation was also increased in AP mice, but it was
decreased by ALR. ALR alleviates acute pancreatitis by inhibiting
HMGB1/TLR4/NF-?B signaling pathway. It is promising to alleviate the syndromes of
patients with acute via targeting ALR.