Synthesis and antifungal activity of 7-methyl-7-hydroxy-2,3-benzo[c]octa-1,6-olide.

The racemic 7-methyl-7-hydroxy-2,3-benzo[c]octa-1,6-olide, the analog of natural product (6R)-3,7-dimethyl-7-hydroxy-2-octen-1,6-olide, was totally synthesized using easily available (E)-2-(2-carboxyvinyl)benzoic acid as a raw material in nine-step reactions including three key steps of Wittig reaction, epoxidation, and cyclization, with an overall yield of 10.3%. The bioassay results showed that ( ± )-2 exhibited stronger antifungal activity than the natural product ( ± )-1 and (R)-1 against Alternaria solani with an EC50 value of 27.36 µg/ml.

Total synthesis of 3,7-dimethyl-7-hydroxy-2-octen-1,6-olide and 3,7-dimethyl-2,6-octadien-1,6-olide.

3,7-Dimethyl-7-hydroxy-2-octen-1,6-olide and 3,7-dimethyl-2,6-octadien-1,6-olide, the natural bioactive compounds isolated from the fruit of Litsea cubeba and the liverwort Plagiochila rutilans, were totally synthesized using easily available cis-geraniol as raw material in short, convenient, and low-cost, five-step reactions including three steps of oxidation, cyclization, and dehydration, with an overall yield of 47.5% and 37.3%.

MiR-491-3p is down-regulated in postmenopausal osteoporosis and affects growth, differentiation and apoptosis of hFOB1.19 cells through targeting CTSS.

BACKGROUND: Postmenopausal osteoporosis (PMO) is a common disease related to aging, which has been paid increasing attention in recent years because of its serious complications. MiR-491-3p was found to play a crucial roles in several diseases. However, the role of miR-491-3p in PMO has yet not been studied. Our research intends to explore the impact of miR-491-3p on PMO in the in vitro model. MATERIAL AND METHODS: The expression patterns of miR-491-3p and cathepsin S (CTSS) in patients with PMO were acquired from the GEO database. The human osteoblast cell hFOB1.19 was used to detect the function of miR-491-3p and CTSS in PMO. The viability and apoptosis of hFOB1.19 cells were measured by cell counting kit 8 and flow cytometry assays. The apoptosis and differentiation related proteins were analyzed by western blotting. The relationship between miR-491-3p and CTSS was predicted by appropriate software and affirmed by luciferase assay. RESULTS: MiR-491-3p expression was lower in patients with PMO. The up-regulation of miR-491-3p in hFOB1.19 cells increased their viability and differentiation and inhibited their apoptosis. CTSS, which was highly expressed in patients with PMO, was confirmed as a direct target of miR-491-3p and was found to be inversely modulated by miR-491-3p. The rescue assays showed that overexpression of CTSS suppressed the promoting effects of miR-491-3p mimic on the proliferation and differentiation of hFOB1.19 cells, and repressed the inhibitory effects of miR-491-3p mimic on apoptosis of hFOB1.19 cells. CONCLUSIONS: The results of our study showed that miR-491-3p could ameliorate biological characteristics of hFOB1.19 cells by reducing CTSS expression suggesting that miR-491-3p/CTSS might be a potential biomarker for the diagnosis and treatment of PMO.