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The purpose of this study was to evaluate the protective effect of pterostilbene (Psb) against lipopolysaccharide and D-galactosamine (L/D)-induced acute liver failure (ALF) in mice and its potential mechanisms. Histology of liver was detected by H&E staining. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in serum and malondialdehyde (MDA), myeloperoxidase (MPO), glutathione (GSH), and superoxide dismutase (SOD) contents in liver were examined using detection kits. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) secretion were detected by ELISA. Meanwhile, MAPK, NF-κB, NLRP3 inflammasome, and Nrf2 were assessed by western blotting. Our findings showed that pretreatment with Psb protected against L/D-induced ALF by lowering the lethality, improving liver histology, reducing ALT, AST, IL-6, IL-1β, TNF-α, MDA, and MPO levels, and boosting liver GSH content and SOD activity. Moreover, Psb pretreatment effectively suppressed inflammation by decreasing NLRP3 inflammasome, MAPK, and NF-κB pathway activations. Moreover, Psb pretreatment efficiently enhanced the expression of several antioxidant enzymes, mainly depending on Nrf2 activation. This was the first study to demonstrate that Psb protects against L/D-induced ALF by inactivating MAPK, NF-κb, and NLRP3 inflammasome and upregulating the Nrf2 signaling pathway, indicating a potential therapeutic application for ALF treatment.
Inflammation is an immune response against avariety of noxious stimuli, such as infection, chemicals,and physical injury. Eugenol, a natural phenolic extract,has drawn much attention for its various desirable pharmacologicalfunctions and is, therefore, broadly used in ourdaily life and medical practice. However, further usage ofeugenol is greatly limited due to its unwanted properties,such as physicochemical instability, poor solubility, andhigh-dose cytotoxicity. In hopes of extending its applicabilitythrough glycosylation, we previously reported anovel, efficient, and high throughput way to biosynthesizea-D-glucosylated eugenol (a-EG). In this study, we furtherexplored the potential superior properties of a-EG to itsparent eugenol in terms of anti-inflammatory activities. Wedemonstrated that a-EG was an effective anti-inflammatorymediator in both non-cellular and cellular environments. In addition, the non-cellular inhibitory effect of a-EGcould be amplified by a-glucosidase, which ubiquitouslyexists in cytoplasm. Furthermore, a-EG exhibited a superior anti-inflammatory effect to its parent eugenol in a cellularenvironment. In words, our findings collectively suggest thata-EG is a stronger anti-inflammatory mediator and maythereby serve as a desirable substitute for eugenol and apotential therapeutic prodrug in treating inflammatory diseasesin the future.
Recently, Li  gave an asymptotic formula for the ultimate ruin probability in a delayed-claim risk model with constant force of interest and pairwise quasi-asymptotically independent and extended-regularly-varying-tailed claims. This paper extends Li's result to the case in which the risk model is perturbed by diffusion, the claims are consistently-varying-tailed and the main-claim interarrival times are widely lower orthant dependent.
An efficient and selective method for the synthesis of ethyl 2-amino/aryloxy-3-aryl-4-oxo-5-phenyl-4,5- dihydro-3H-pyrrolo[3,2-d]pyrimidine-7-carboxylate derivatives has been developed. The main process involved the reaction of diethyl 1-phenyl-3-((triphenylphosphoranylidene)amino)-1H-pyrrole-2,4-dicarboxylate and aromatic isocyanates, followed by addition of amines/phenols in the presence of catalytic amount of sodium ethoxide or solid potassium carbonate.
Cisplatin is a platinum-based compound that islargely employed as an effective antitumor drug against awide spectrum of solid neoplasms for many years. Despiteof its initial therapeutic success, cisplatin often results inhigh incidence of chemoresistance and high-dose cytotoxicity. Consequently, considerable efforts in hopes ofreducing the dose-dependent side effects of cisplatin whileretaining, or even enhancing, its antitumor properties havebeen undertaken throughout the past three decades. Nitricoxide (NO) is a small lipophilic free radical gas possessingversatile biological functions, including antitumor activities. However, NO, of itself, is difficult to be used, becauseof its extreme instability and short half-life. Previously, wehave reported a stable NO donor, b-galactosyl-pyrrolidinyldiazeniumdiolate (b-Gal-NONOate), which exerts tumorkilling effects through site-specific intracellular release ofexogenous NO. In this study, we further investigated thecombined inhibitory effect of b-Gal-NONOate and cisplatinagainst C6/LacZ, 9L/LacZ, and HeLa/LacZ tumorcells. It was shown that, in combination with b-Gal-NONOate, the antitumor effects of cisplatin against thesecommon tumor cell lines were increased in a dose-dependentmanner. Furthermore, the combination of thesechemicals resulted in a synergistic suppression on tumorgrowth, which was achieved under a much lower cisplatindosage. Collectively, our findings indicate that b-Gal-NONOate can synergistically improve the antitumor effectof cisplatin, and may therefore reduce its side effectscaused by high dose cisplatin monochemotherapies. Accordingly, b-Gal-NONOate is an important therapeuticassistant reagent with great potential of clinical applicability,and thus worth of continuous research in the comingfuture.
Recently, Li  gave an asymptotic formula for the ultimate ruin probability in a delayed-claim risk model with constant force of interest and pairwise quasi-asymptotically independent and extendedregularly- varying-tailed claims. This paper extends Li's result to the case in which the risk model is perturbed by diffusion, the claims are consistently-varying-tailed and the main-claim interarrival times are widely lower orthant dependent.