Plastic pollution is ubiquitous and not even remote protected islands are safe from it Floating debris can adsorb toxic compounds that concentrate on their surface, being available to the animals that ingest them For this reason, a baseline study of plastic pollution was conducted in the remote Revillagigedo Archipelago, in the Mexican Pacific Ocean In 47 manta net samples an average of 48 plastics/1000m2 was found, 73 of the pieces being less then 5 mm Polyethylene and polypropylene were the most common polymers found The chemical analysis of organic pollutants revealed that organochlorine pesticides, polycyclic aromatic hydrocarbons and polychlorinated biphenyls are adsorbed on the plastics collected in the area Filter feeding megafauna such as humpback whales, manta rays and whale sharks could ingest contaminated micro and macroplastics Plastics were found also on the beach, where they are available to the ingestion by terrestrial animals, including endemic species endangered to extinctionThe antipsychotic drug olanzapine was reported to induce nonalcoholic fatty liver disease NAFLD, whereas the underlying mechanism remains incompletely understood This study investigated whether apolipoprotein A5 apoA5 and sortilin, two interactive factors involved in NAFLD pathogenesis, are implicated in olanzapine-induced NAFLD  https//wwwselleckchemcom/products/pcna-i1html  In our study, at week 8, olanzapine treatment successfully induced hepatic steatosis in female C57 BL/6 J mice, which was independent of body weight gain Likewise, olanzapine effectively mediated hepatocyte steatosis in HepG2 cells characterized by substantially elevated intracellular lipid droplets Increased plasma triglyceride concentration and decreased plasma apoA5 levels were observed in mice treated with 8-week olanzapine Surprisingly, olanzapine markedly enhanced hepatic apoA5 protein levels in mice, without a significant effect on rodent hepatic ApoA5 mRNA Our in vitro study showed that olanzapine reduced apoA5 protein levels in the medium and enhanced apoA5 protein levels in hepatocytes, whereas this drug exerted no effect on hepatocyte APOA5 mRNA By transfecting APOA5 siRNA into HepG2 cells, it was demonstrated that APOA5 knockdown effectively reversed olanzapine-induced hepatocyte steatosis in vitro In addition, olanzapine drastically increased sortilin mRNA and protein levels in vivo and in vitro Interestingly, SORT1 knockdown reduced intracellular apoA5 protein levels and increased medium apoA5 protein levels in vitro, without affecting intracellular APOA5 mRNA levels Furthermore, SORT1 knockdown greatly ameliorated hepatocyte steatosis in vitro This study provides the first evidence that sortilin inhibits the hepatic apoA5 secretion that is attributable to olanzapine-induced NAFLD, which provides new insight into effective strategies against NAFLD for patients with schizophrenia administered olanzapineNLRP3 inflammasome is a key mediator in ischemic stroke-induced neuroinflammation and subsequent brain injury Our previous study demonstrated the potent activity of Pien-Tze-Huang PTH, a well-known Chinese patent formula, in reducing mitochondria-mediated neuronal apoptosis in cerebral ischemia/reperfusion impaired rats This study aims to elucidate the mechanistic action of PTH related to neuroinflammation in LPS-induced BV2 microglial cells and cerebral ischemia/reperfusion impaired rats BV2 cells were stimulated with LPS for 12 h and treated with PTH with various concentrations Modulation by PTH of relevant genes IL-6, IL-1β, IL-18, TNF-α, COX-2 and iNOS mRNA and proteins NLRP3 inflammasome, autophagy and AMPK/mTOR/ULK signaling was analyzed by real-time PCR and western blot, respectively Similar analyses were conducted in middle cerebral artery occlusion rat model including neurological deficit, infarct volume, microglial activation, and key genes and proteins in modulating autophagy and NLRP3 Our results showed that PTH significantly inhibited the production of key proinflammatory mediators and protein expressions of NLRP3 and caspase-1 p20 in LPS induced BV2 cells It also enhanced the autophagy response by modulating the key autophagy proteins via AMPK/mTOR/ULK related pathway The reduced inflammatory responses and NLRP3 expressions by PTH were partially blocked by the autophagy inhibitor 3-MA and AMPK blocker compound C In rats, PTH significantly reduced infarct size, suppressed microglial activation, and improved neuron deficit It also promoted autophagy and reduced NLRP3 activity Our study demonstrated that PTH inhibited NLRP3 inflammasome-mediated neuroinflammation, which was associated with enhanced autophagy via AMPK/mTOR/ULK1 pathway in vitro and in vivoThymic stromal lymphopoietin TSLP produced by mast cells is involved in allergic inflammation pathogenesis Chloroquine CQ is known to be an anti-malarial drug; however, additional protective functions of CQ have been discovered This study aims to clarify an anti-inflammatory effect of CQ through modulating TSLP levels using an in vitro model of phorbol myristate acetate PMA + A23187-activated human mast cell line HMC-1 and an in vivo model of PMA-irritated ear edema CQ treatment reduced the production and mRNA expression levels of TSLP in activated HMC-1 cells CQ down-regulated caspase-1 CASP1, MAPKs, and NF-κB levels enhanced by stimulation with PMA + A23187 Moreover, ear thickness in ear edema was suppressed following CQ treatment CQ decreased CASP1 and NF-κB levels in the ear tissue TSLP levels in the ear tissue and serum were reduced following CQ treatment Collectively, the above findings elucidate that CQ inhibits the pro-inflammatory mechanisms of TSLP via the down-regulation of distinct intracellular signaling cascade in mast cells Therefore, CQ may have protective roles against TSLP-mediated inflammatory disordersLung cancer treatment using cisplatin DDP in combination with other drugs are effective for the treatment of non-small cell lung cancer NSCLC The aim of this study was to prepare a layer-by-layer nanoparticles NPs for the co-loading of DDP and oridonin ORI and to evaluate the antitumor activity of the system in vitro and in vivo Novel DDP and ORI co-loaded layer-by-layer NPs D/O-NPs were constructed The mean diameter, surface change stability and drug release behavior of NPs were evaluated In vitro cytotoxicity of D/O-NPs was investigated against DDP resistant human lung cancer cell line A549/DDP cells, and in vivo anti-tumor efficiency of D/O-NPs was tested on mice bearing A549/DDP cells xenografts D/O-NPs have a diameter of 1396 ± 44 nm, a zeta potential value of +138 ± 16 mV D/O-NPs could significantly enhance in vitro cell toxicity and in vivo antitumor effect against A549/DDP cells and lung cancer animal model compared to the single drug loaded NPs and free drugs The results demonstrated that the D/O-NPs could be used as a promising lung cancer treatment systemPlant-based natural extracts contain several nutrients and bioactive compounds, such as phenolics and flavonoids, that possess various health-promoting activities This study investigated the effects of polyphenols from Pterocarpus santalinus hydroalcoholic extract PSHE against gamma radiation-induced derangements via the upregulation of Nrf2 Ultra High Performance Liquid Chromatography Coupled to High Resolution Mass Spectrometry UHPLC-HRMS/MS analysis was performed to identify the possible radioprotectors In vivo and in vitro studies, namely Real-Time-PCR RT-PCR analysis, Reactive Oxygen Species ROS scavenging activity, lipid peroxidation and GSH levels, DNA damage and cell death studies, anti-inflammatory Sandwich ELISA, immunomodulatory studies antibody staining, and model free radical scavenging assays, were performed Vanillic acid, protocatechuic acid, para-hydroxybenzoic acid, chlorogenic acid, TNF-α inhibitor Eudesmin, isoflavone Daidzein 7-o-glucoside, astragalin Kaempferol 3-o-glycoside, and other polyphenols were identified in PSHE using UHPLC-HRMS/MS analysis Prophylactic administration of PSHE -1 h rendered more than 33 survival in mice exposed to 8 Gy whole-body-irradiation with increased mice survival and recovery of bone marrow and spleen cellularity Real-time RT-PCR analysis showed that PSHE treatment 50 µg/mL upregulated Nrf2, HO-1, and GPX-1 in mice splenocytes At 50 µg/mL, PSHE reduced ROSscavenging activity, mitochondrial and spleen membrane lipid peroxidation levels, DNA damage, and cell death, and increased GSH levels At 10 µg/mL, PSHE treatment diminished the content of IL-6 and TNF-α At 50 µg/mL, PSHE suppressed lymphocyte proliferation These findings indicate that polyphenols of PSHE possess marked antioxidant, anti-inflammatory, and immunomodulatory capacities, which play important roles in the prevention of radiation damageAtrophy is defined as a reduction in cell, organ, or tissue size after reaching their normal mature sizes because of loss of organelles, cytoplasmic compartments, and proteins This process is also involved in the pathogenesis of human disorders Inadequate nourishment, poor circulation, inadequate hormonal support, defects in nerve supply of the tissue, disproportionate induction of apoptosis in the tissue, and absence of exercise are some underlying causes of atrophy Recently, several non-coding RNAs ncRNAs have been identified that regulate atrophy, thus participating in the pathobiology of related disorders such as neurodegenerative/ neuromuscular diseases, age-related muscle atrophy, and cardiac tissue atrophy In the current review, we have focused on two classes of ncRNAs namely long ncRNAs lncRNAs and microRNAs miRNAs to unravel their participation in atrophy-associated disordersA mild ischemic stroke may cause both debilitating locomotor and cognitive decline, for which the mechanism is not fully understood, and no therapies are currently available In this study, a nonfatal stroke model was constructed in mice by a modified middle cerebral artery occlusion MCAO procedure, allowing an extended recovery period up to 28 days The extended MCAO model successfully mimicked phenotypes of a recovery phase post-stroke, including locomotor motor and cognitive deficiencies, which were effectively improved after Shuxuening injection SXNI treatment Tissue slices staining showed that SXNI repaired brain injury and reduced neuronal apoptosis, especially in the hippocampus CA3 region Transcriptomics sequencing study revealed 565 differentially expressed genes DEGs in the ischemic brain after SXNI treatment Integrated network pharmacological analysis identified Neurotrophin/Trk Signaling was the most relevant pathway, which involves 15 key genes Related DEGs were further validated by RT-PCR Western-blot analysis showed that SXNI reversed the abnormal expression of BDNF, TrkB, Mek3 and Jnk1after stroke ELISA found that SXNI increased brain level of p-Erk and Creb At sub-brain level, the expression of BDNF and TrkB was decreased and GFAP was increased on the hippocampal CA3 region in the post-stroke recovery phase and this abnormality was improved by SXNI In vitro experiments also found that oxygen glucose deprivation reduced the expression of BDNF and TrkB, which was reversed by SXNI In summary, we conclude that SXNI facilitates the recovery of cognitive and locomotor dysfunction by modulating Neurotrophin/Trk Signaling in a mouse model for the recovery phase of post-ischemic stroke