One new phenalenone derivative, peniciherqueinone (1), together with five known phenalenone derivatives (2–6), one known anthraquinone (7) and two known acetophenones (8 and 9) were isolated from the soil fungus Penicillium herquei PSU-RSPG93. Their structures were established by spectroscopic evidence. The absolute configuration of 1 was determined by anisotropic effect and electronic circular dichroism spectroscopy. Compound 2 exhibited mild antioxidant activity and is noncytotoxic to Vero (African green monkey kidney fibroblasts) cell lines.

Hydrolytic and enzymatic degradation of resin adhesives over time has been mainly attributed to secondary caries formation of methacrylate-based tooth-colored resin-based composite restorations. Ability of resin adhesive monomers to infiltrate into demineralized dentin forming stiff polymer matrix and potentially bonding to tooth structure is also a crucial property. The only commercially available antibacterial monomer, 12-methacryloyloxydodecyl pyridinium bromide (MDPB), is a quaternary ammonium methacrylate. This methacrylate monomer undergoes hydrolytic degradation, and could not bond to tooth structure. In this study, a new hydrolytic resistant monomer HMTAF was synthesized. It is methacrylamide-based monomer that, unlike methacrylate, is highly resistant to hydrolysis. Its molecular structure has particular functional groups; quaternary ammonium fluoride salt with potential antibacterial fluoride-releasing activity, hydroxyl and amide group with hydrogen bonding potential to dentin collagen. Hydroxyl group also increases monomer hydrophilicity for better penetration into water-saturated dentin and sufficient resin-dentin bond. The synthesized HMTAF and its polymer showed no hydrolytic degradation in acidic environment, while MDPB and its polymer were partially decomposed under this challenge. The conversion of monomer HMTAF to polymer was illustrated by FT-IR. The results indicated that HMTAF is highly resistant to hydrolysis, polymerizable and non-cytotoxic to Vero cell lines. It is a potential monomer to be incorporated into resin adhesives for improving hydrolytic and enzymatic resistance.

Isolated α,β-dehydromonacolin S (C5) from soil-derived fungus Aspergillus sclerotiorum PSU-RSPG178 was recently shown to exhibit an inhibitory effect against 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) activity in vitro. In this study, we investigated the effects of C5 on lipid-lowering, hepatic steatosis, and hepatic gluconeogenesis in vivo. The control rats received a daily dose of either vehicle or C5 at 10 mg/kg, while the high-fat diet-induced obese (HFD) rats were administered vehicle; 1, 3, or 10 mg/kg C5; or 10 mg/kg lovastatin (LO) for 6 weeks. C5 significantly improved dyslipidemia and diminished liver enzymes, HMGR activity, insulin resistance, and hepatic steatosis, comparable to LO without any hepatotoxicity and nephrotoxicity in HFD rats. A higher efficacy of C5 in lipid-lowering activity and anti-hepatic steatosis was associated with a significant decrease in genes involved in lipid metabolism including sterol regulatory element binding protein (SREBP) 1c, SREBP2, liver X receptor alpha (LXRα), and peroxisome proliferator-activated receptor (PPAR) gamma (PPARγ) together with an increase in the PPAR alpha (PPARα). Correspondingly, C5 was able to down-regulate the lipid transporters cluster of differentiation 36 (CD36) and Niemann-Pick C1 Like 1 (NPC1L1), increase the antioxidant superoxide dismutase gene expression, and decrease the proinflammatory cytokines, tumor necrosis factor alpha (TNFα) and interleukin 1 beta (IL-1β). Impairment of hepatic gluconeogenesis and insulin resistance in HFD rats was restored by C5 through down-regulation of the gluconeogenic genes phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase), and the activation of AMP-dependent kinase serine (AMPK) and serine/threonine protein kinase B (Akt). Collectively, this novel C5 may be a therapeutic option for treating dyslipidemia, hepatic steatosis, and reducing potential risk for diabetes mellitus.