This paper describes the development of a film comprising chitosan (CS), sodium alginate (SA), and ethyl cellulose (EC) for buccal mucosal administration. A film of CS-SA unidirectional release drug-containing water-repellent layer EC was produced by interfacial reaction solvent-drying technique using self-made equipment. The CS-SA-EC film had superior mechanical properties compared to CS-EC and SA-EC films. The existence of the amide bond was confirmed by FT-IR. DSC confirmed that the drug was dispersed in the carrier material in an amorphous form. The drug release studies emerged that the model drugs from CS-SA-EC films presented better release properties. The Ritger-Peppas model best describes all ratios of drugs release mechanisms. The permeability characteristics of the films were evaluated in the TR146 cells model and the rabbit buccal mucosae. The cumulative penetration amounts of the model drugs were significantly increased. The permeability mechanism of the film was studied preliminarily using immunofluorescence and Western Blot. The results showed that the film inhibited the expression of ZO-1 protein, and the expressive trend of ZO-1 protein was consistent with the results of in vitro permeation experiments. The pharmacokinetics of the drugs loaded films were evaluated and compared with oral administration in rats. The relative bioavailability of the model drugs was 246.00% (Zolmitriptan) and 142.12% (Etodolac) relative to oral administration. The results of this study demonstrate the potential of CS-SA-EC vehicle in buccal mucosa drug delivery.

Liver inflammation and excessive accumulation of lipids play a critical role in alcoholic liver diseases (ALD) pathogenesis. Plant polyphenols are widely used to prevent toxic liver damage. The anthocyanin from Lonicera caerulea L. was extracted and purified. The aim of the study was to evaluate the hepatoprotective mechanism of the purified component (PLE), focusing on the effects of PLE on alcoholic steatohepatitis. C57BL/6 mice were fed on chronic plus binge ethanol in Lieber-DeCarli liquid diet to establish acute ethanol model. PLE treatment significantly reduced the accumulation of serum aminotransferase and triglycerides and increased albumin levels in ethanol-induced mice. Also, PLE ameliorated histological changes and lipid droplets induced by ethanol. In addition, PLE obviously suppressed the expression of SREBP1 and enhanced phosphorylation of AMPK compared with chronic ethanol administration. PLE suppressed inflammasome activation by decreasing F4/80 level and inhibiting caspase-1, thereby preventing activated macrophages from producing pro-inflammation cytokines. AML12 cells were pretreated with different concentrations of PLE for 2 h and then exposed to ethanol for 48 h. PLE suppressed the expression of SREBP1 and enhanced phosphorylation of AMPK in AML12 cells exposed to ethanol. Additionally, PLE inhibited the expression of F4/80 and decreased IL-1β release. AMPK interference confirms that PLE downregulation SREBP1 and F4/80 depending on AMPK activation in ethanol-treated AML12 cells. PLE possessed the capacity for inhibiting the inflammatory response and suppressing lipid accumulation, indicating that PLE can be used as a dietary health supplement for alcoholic steatohepatitis.