[HTML][HTML] Involvement of the PI3K/Akt/NF-κB Signaling Pathway in the Attenuation of Severe Acute Pancreatitis-Associated Acute Lung Injury by Sedum sarmentosum …

Y Jin, L Liu, B Chen, Y Bai, F Zhang, Q Li… - BioMed Research …, 2017 - hindawi.com
Y Jin, L Liu, B Chen, Y Bai, F Zhang, Q Li, C Lv, H Sun, J Li, S Rubby, L Yang, R Andersson…
BioMed Research International, 2017hindawi.com
Sedum sarmentosum Bunge possesses excellent anti-inflammatory properties and was
used in the treatment of inflammatory diseases. The aim of the present study was to
investigate the efficiency of Sedum sarmentosum Bunge extract (SSBE) on severe acute
pancreatitis-associated (SAP-associated) acute lung injury (ALI) in rats and to explore the
underlying mechanisms. Here, we used a sodium taurocholate-induced SAP rat model to
determine the role of SSBE in ALI. During the course of pancreatitis, the expressions of …
Sedum sarmentosum Bunge possesses excellent anti-inflammatory properties and was used in the treatment of inflammatory diseases. The aim of the present study was to investigate the efficiency of Sedum sarmentosum Bunge extract (SSBE) on severe acute pancreatitis-associated (SAP-associated) acute lung injury (ALI) in rats and to explore the underlying mechanisms. Here, we used a sodium taurocholate-induced SAP rat model to determine the role of SSBE in ALI. During the course of pancreatitis, the expressions of phosphorylated phosphoinositide 3-kinases (PI3K)/protein kinase B (Akt) and nuclear factor-kappa B (NF-κB) p65 in the lungs were upregulated. Meanwhile, a parallel increase in the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in the lungs was observed after the induction of SAP. Treatment with SSBE significantly reduced the expression of p-Akt and p-p65 in the lungs and attenuated the severity of SAP-associated ALI compared to the SAP group at 12 h and 24 h. In summary, this study showed that SSBE has beneficial effects on SAP-associated ALI, probably through the PI3-K/Akt signaling pathways by suppressing the NF-κB activities.
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