The Properties of Modified Bagasse Fiber/Nano-TiO2 Composite Asphalt in a High-Temperature and High-Humidity Salt Environment.

The southern tropical coastal areas of China are high-temperature and high-humidity salt environments, which hinder the durability and service life of ordinary asphalt pavement. To enhance the durability of asphalt pavement in these areas, modified bagasse fiber combined with nano-TiO2 was used to improve the corrosion resistance of asphalt pavement in high-temperature and high-humidity salt environments. The micro-morphology, high-temperature oil absorption, high-temperature heat resistance, and hygroscopicity of bagasse fiber modified using three silane coupling agents combined with NaOH were compared, and the best silane coupling agent/NaOH modification scheme for bagasse fiber was found. Based on conventional physical tests (penetration, softening point, ductility), rheological property tests (rotational viscosity, dynamic shear rheological test, multi-stress creep recovery test, linear amplitude scanning test), and a four-point bending fatigue test of the asphalt mixture, the properties of modified bagasse fiber asphalt binder and mixture after cyclic dry-wet erosion under pure water and salt solution (NaCl, Na2SO4) were determined, and the effects of the erosion environment and fiber ratio on the basic physical and rheological properties of the asphalt were clarified. Compared with the silane coupling agents KH550 and KH590, the bagasse fiber modified with KH570/NaOH had a better high-temperature oil absorption capacity, heat stability capacity, and matrix asphalt compatibility. The worst erosion environment was Na2SO4, but the increase in test temperature and fiber content weakened the sensitivity of the asphalt binder performance in different erosion environments. The erosion capacity order was as follows: Na2SO4 > NaCl > pure water. In the worst erosion environment, 0.5% modified bagasse fiber/Nano-TiO2 asphalt binder (Bn-570-0.5) had the best corrosion resistance in a high-temperature and high-humidity salt environment. The penetration, softening point, creep recovery rate R3.2, non-recoverable creep compliance Jnr3.2, and fatigue life after long-term aging (with 5% strain) of Bn-570-0.5 were, respectively, increased by -16.9%, 37.5%, 37.95%, -27.86%, and 38.30% compared with unblended base asphalt binder (B). In addition, the four-point flexural fatigue life of Bn-570-0.5 was 169.2% higher than that of the unblended base mixture.

Puerarin inhibited 3-chloropropane-1,2-diol fatty acid esters formation by reacting with glycidol and glycidyl esters.

The inhibitory effects of seven polyphenols on 3-chloropropane-1,2-diol fatty acid esters (3-MCPDE) formation were investigated in palm oil models. Results showed that there was not a positive significant correlation between the free-radical scavenging activities of the tested compounds and their 3-MCPDE-formation inhibitory activities; puerarin, with weak antioxidant activity, showed the highest inhibitory capacity. Moreover, puerarin reduced the content of glycidol and glycidyl esters (GEs), two key intermediates of 3-MCPDE formation in the oil models; and a puerarin-adduct was discovered in the oil fortified with glycidol or GEs, with its structure elucidated by LC-MS/MS and comparison with newly synthesized ones. Based on its chemical structure, we proposed that puerarin, at least in part, reacted with glycidol and GEs to inhibit 3-MCPDE formation. In addition, the formed compound, puerarin-7-O-propanediol was identified in the potato chips frying system, further confirming reacting with glycidol/GEs as a key mechanism of puerarin to inhibit 3-MCPDE formation.

4'-Methoxyresveratrol Alleviated AGE-Induced Inflammation via RAGE-Mediated NF-κB and NLRP3 Inflammasome Pathway.

Advanced glycation end products (AGEs) could interact with the receptor for AGE (RAGE) as a sterile danger signal to induce inflammation. 4'-methoxyresveratrol (4'MR), a polyphenol derived from Dipterocarpaceae, has not been studied for its anti-inflammation effects. In the present study, we sought to explore the protective role of 4'MR in AGEs-induced inflammatory model using RAW264.7 macrophages. 4'MR significantly inhibited gene expression of pro-inflammatory cytokines and chemokines, such as interleukin 1ß (IL-1ß), interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-α) and monocyte chemoattractant protein-1 (MCP-1), as well as two typical pro-inflammatory enzymes, inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2). Besides, 4'MR significantly decreased oxidative stress, demonstrated by levels of ROS production, protein carbonyl and advanced oxidation protein product via down-regulation of NADPH oxidase. Further analysis showed that 4'MR attenuated the RAGE overexpression induced by MGO-BSA. It also blocked the downstream signal of AGE-RAGE, particularly, MAPKs including p38 and JNK, and subsequently reduced NF-κB activation. Additionally, 4'MR significantly abated the activation of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome including NLRP3 and cleaved caspase-1 and reduced the secretion of mature IL-1ß. Taken together, our results suggest that the anti-inflammatory effect of 4'MR is mainly through suppressing RAGE-mediated MAPK/NF-κB signaling pathway and NLRP3 inflammasome activation. 4'MR could be a novel therapeutic agent for inflammation-related diseases.