Enhancing Stiffness and Oil Resistance of Fluorosilicone Rubber Composites through Untreated Cellulose Reinforcement.

Fluorosilicone rubber, essential in automotive and aerospace owing to its excellent chemical resistance, plays a pivotal role in sealing technology, addressing the industry's evolving demands. This study explores the preparation and properties of fibrillated cellulose-reinforced fluorosilicone rubber composites to enhance their stiffness and oil resistance. Fibrillated cellulose sourced as a wet cake and subjected to processing and modification is incorporated into a fluorosilicone rubber matrix. The resulting composites are analysed by tensile and compression tests, along with compressive stress-relaxation testing in air and in an oil-immersed environment. The findings demonstrate significant improvements in the mechanical properties, including an increased Young's modulus and elongation at break, whereas the tensile strength remained uncompromised throughout the testing procedures. Morphological analysis of the fracture surfaces revealed a remarkable interfacial affinity between the fibrillated cellulose and rubber matrix, which was attributed in part to the modified fatty acids and inorganic nanoparticles. The presence of fibrillated cellulose enhanced the stress-relaxation characteristics under oil-immersion conditions. These results contribute to the domain of advanced elastomer materials, with potential for applications requiring enhanced mechanical properties and superior oil resistance.

Cynandione A from Cynanchum wilfordii inhibits hepatic de novo lipogenesis by activating the LKB1/AMPK pathway in HepG2 cells.

Cynandione A (CA), isolated from ethyl acetate extract of Cynanchum wilfordii (CW), is a bioactive phytochemical that has been found to be beneficial for the treatment of several diseases. Hepatic de novo lipogenesis is one of the main causes of non-alcoholic fatty liver disease (NAFLD), which is thought to be a hepatic manifestation of certain metabolic syndromes. However, it has not yet been reported if CA has any therapeutic value in these diseases. Here, we investigated whether CA can inhibit hepatic lipogenesis induced by liver X receptor α (LXRα) using an in vitro model. We found that the extract and ethyl acetated layer of CW decreased the mRNA levels of sterol regulatory element-binding protein-1c (SREBP-1c), which plays a crucial role in hepatic lipogenesis. Additionally, we observed that CA could suppress the level of SREBP-1c, which was increased using two commercial LXRα agonists, GW3954 and T0901317. Moreover, the enzymes that act downstream of SREBP-1c were also inhibited by CA treatment. To understand the mechanism underlying this effect, the levels of phosphorylated AMP kinase (pAMPK) were measured after CA treatment. Therefore, CA might increase the pAMPK level by inducing phosphorylation of liver kinase B1 (LKB1), which can then convert AMPK to pAMPK. Taken together, we conclude that CA has an alleviative effect on hepatic lipogenesis through the stimulation of the LKB1/AMPK pathway.