Abstract
Alisol F and 25-anhydroalisol F isolated from Alisma orientale, were proved to exhibit anti-inflammatory potential in our previous work. In the current study, the anti-inflammatory effects and action mechanisms of alisol F and 25-anhydroalisol F were investigated in vitro. Moreover, the pharmacological effects of alisol F in lipopolysaccharide (LPS)/d-galactosamine (d-gal)-induced acute liver-injured mice were evaluated. The results demonstrated that alisol F and 25-anhydroalisol F could suppress LPS-induced production of nitric oxide (NO), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and interleukin-1β (IL-1β), as well as inhibit the mRNA and protein levels of inducible nitric oxide (iNOS) and cyclooxygenase-2 (COX-2). In addition, we investigated the role of alisol F and 25-anhydroalisol F in mediating mitogen-activated protein kinases (MAPKs), signal transducers, and activators of transcription 3 (STAT3) and nuclear factor κB (NF-κB) pathways involved in the inflammation process of LPS-stimulated RAW 264.7 cells. The phosphorylation of ERK, JNK, p38, and STAT3, and the NF-κB signaling pathway, were obviously suppressed in alisol F and 25-anhydroalisol F treated cells. Results obtained from in vitro experiments suggested alisol F obviously improved liver pathological injury by inhibiting the production of TNF-α, IL-1β, and IL-6, and significantly decreasing the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in LPS/d-gal-induced mice. Furthermore, the reduction of phosphorylation of ERK and JNK, as well as suppression of the NF-κB signaling pathway, were also observed in liver tissues of the alisol F-treated mice model. Alisol F and 25-anhydroalisol F may serve as potential leads for development of anti-inflammatory agents for acute liver failure treatment.
Highlights
Inflammation is a complex defense process caused by many factors, such as chemical stimulus, physical damage, and bacterial infections [1]
Our prior work have demonstrated that alisol F and 25-anhydroalisol F had ability to inhibit the
Our prior work have demonstrated that alisol F and 25-anhydroalisol F had ability to inhibit the production of nitric oxide (NO)
Summary
Inflammation is a complex defense process caused by many factors, such as chemical stimulus, physical damage, and bacterial infections [1]. Lipopolysaccharide (LPS)/D-galactosamine (D-gal) are usually used to establish the experimental animal models of acute hepatic failure [6,8]. Janus kinase/signal transducers and activators of transcription animal models of acute hepatic failure [6,8]. -gal acted as the hepatotoxic or liver damaging as a remedy for hyperlipidemia, hyperglycemia, and inflammatory diseases in China [13]. The ethanol extract of A. and exhibited a number of biological activities, such as antivirus, antitumor, hepato-protective, orientale had been proved to reduce the acute lung inflammation by suppressing the NF-κB [14]. Of biological activities, triterpenes, such as antivirus, hepato-protective, and anti-inflammatory in lipopolysaccharide (LPS)-stimulated [15,20]. F, isolatedinfrom orientale exhibited activities [21] In and protection these two compounds vitroA.and in vivo, using anti-inflammatory. In vitro and in vivo, using LPS-stimulated RAW 264.7 cells and LPS/D-gal-induced liver injury in mice
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
