Objective        To determine the role of sodium-calcium exchanger-1 (NCX1) in the pathogenesis and development of acute pancreatitis (AP).        Methods        Pancreatic acinar cells were isolated and cultured from SD rats

and the obtained pancreatic acini were then treated with caerulein (10

-7

mol/L) for 60 min to induce AP. Quantitative RT-PCR and Western blotting were used to detect th

e expression of NCX1

TNF-α and IL-6 at mRNA and protein levels respectively. After the addition of the specific inhibitor of NCX1

KB-R7943 in the culture medium

the expression levels of above 3 molecules were measured again. SD rats were randomly divided into negative control

caerulein group (AP model group)

and caerulein and KB-R7943 treatment group. After the establishment of AP model

quantitative RT-PCR was used to detect the mRNA levels of NCX1

TNF-α and IL-6 in the splenic tissues of every group. The biochemical analyzer was employed to test the content of serum amylase. Histological changes of the pancreas were observed after HE staining.       Results        The in vitro study indicated that the mRNA and protein levels of NCX1

TNF-α and IL-6 were significantly higher in the AP model group than the negative control (P0.01). While

the specific inhibitors of NCX1

KB-R7943 resulted in significantly suppressed inflammatory responses

and obviously inhibited expression of NCX1

TNF-α and IL-6 at mRNA and protein levels (P0.05). What’s more

the in vivo study also indicated the AP rats had significantly higher mRNA levels of the above 3 molecules (P0.01) and higher serum amylase content (P0.01) when compared with control rats. However

the treatment of the NCX1 inhibitor effectively reversed the above phenomena (P0.01). Morphological observation displayed that the treatment of NCX1 inhibitor obviously attenuated the inflammatory changes induced by caerulein.       Conclusion        NCX1 is involved in the pathogenesis and development of AP

indicating that it might be regarded as the treatment target of AP.