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Computational life sciences, Bioinformatics and System Biology

Berberine hydrochloride mitigates acute pancreatitis by suppressing the TLR4/IκBα/NFκB pathway

, , , , , , , , , & show all
Pages 276-285 | Received 10 Mar 2020, Accepted 02 May 2020, Published online: 29 May 2020
 

Abstract

Severe acute pancreatitis (SAP) usually causes multiple-organ dysfunction syndrome and exhibits a high mortality rate. It has been previously reported that berberine, as a dominant alkaloid, can be effectively used against inflammation. However, there is limited data on the effects of berberine hydrochloride (BBRH) on inflammation in SAP rat models. Male Sprague–Dawley rats were given preliminary intraperitoneal injections of BBRH 30 min prior to retrograde infusion of 5% sodium taurocholate in their biliopancreatic ducts. The rats were sacrificed 12 h after taurocholate administration, and tissues and blood samples were then acquired for histological, chemical, and molecular analyses. The SAP models exhibited enhanced edema, ascitic fluid volume, neutrophil infiltration, serum amylase and lipase levels, and interleukin (IL)-6, tumor necrosis factor-α, and IL-1β levels, and reduced IL-10 concentration, while BBRH administration reversed these changes. Further study showed that in the SAP model, protein and mRNA levels of nuclear factor kappa-light-chain-enhancer of activated B (NFκB) p65 and toll-like receptor 4 (TLR4) were increased and inhibitor of nuclear factor kappa B (IκBα) expression was decreased, while pretreatment with BBRH significantly decreased the activation of the TLR4/IκBα/NFκB pathway. The data obtained displayed that BBRH mitigated acute pancreatitis by suppressing the TLR4/IκB/NFκB pathway.

Data availability statement

The raw data required to reproduce these findings cannot be shared at this time as the data also forms part of an ongoing study.

Disclosure statement

No potential conflict of interest was reported by the author(s).