Macrophage β-arrestin-1 deteriorates DSS-induced colitis through interaction with NF-κB signaling.

β-arrestin-1 has been demonstrated to participate in the regulation of inflammatory reactions in several diseases. Thus, this study aimed to investigate the role of macrophage β-arrestin-1 in the pathogenesis and progression of ulcerative colitis (UC). A myeloid β-arrestin-1 conditional knockout mouse model was generated to explore the role of macrophage β-arrestin-1.

Combined administration of anisodamine and neostigmine alleviated colitis by inducing autophagy and inhibiting inflammation.

Our previous work demonstrated that the anisodamine (ANI) and neostigmine (NEO) combination produced an antiseptic shock effect and rescued acute lethal crush syndrome by activating the α7 nicotinic acetylcholine receptor (α7nAChR). This study documents the therapeutic effect and underlying mechanisms of the ANI/NEO combination in dextran sulfate sodium (DSS)-induced colitis. Treating mice with ANI and NEO at a ratio of 500:1 alleviated the DSS-induced colitis symptoms, reduced body weight loss, improved the disease activity index, enhanced colon length, and alleviated colon inflammation.

Depletion of β-arrestin-1 in macrophages enhances atherosclerosis in ApoE mice.

Autophagy in atherosclerotic plaque macrophage contributes to the alleviation of atherosclerosis through the promotion of lipid metabolism. β-arrestins are multifunctional proteins participating various kinds of cellular signaling pathways. Here we aimed to determine the role of β-arrestin-1, an important member of β-arrestin family, in atherosclerosis, and whether autophagy was involved in this process.

The critical role of ferritinophagy in human disease.

Ferritinophagy is a type of autophagy mediated by nuclear receptor activator 4 (NCOA4), which plays a role in inducing ferroptosis by regulating iron homeostasis and producing reactive oxygen species in cells. Under physiological conditions, ferritinophagy maintains the stability of intracellular iron by regulating the release of free iron. Studies have demonstrated that ferritinophagy is necessary to induce ferroptosis; however, under pathological conditions, excessive ferritinophagy results in the release of free iron in large quantities, which leads to lipid peroxidation and iron-dependent cell death, known as ferroptosis.

Magnetic chitosan microspheres: An efficient and recyclable adsorbent for the removal of iodide from simulated nuclear wastewater.

The efficient and recyclable magnetic chitosan microspheres (MCMs) were successfully synthesized to remove iodide from nuclear wastewater and characterized through XRD, FTIR, SEM, EDS, VSM, TGA and XPS. The characterization results indicated that the MCMs exhibited smooth spherical morphology and good magnetic properties. The removal potential of MCMs was investigated for iodide (I) anions at different conditions.

Clinical Efficacy of Immune Checkpoint Inhibitors in Non-Small Cell Lung Cancer Patients with Liver Metastases: A Network Meta-Analysis of Nine Randomized Controlled Trials.

Purpose: This network meta-analysis (NMA) was conducted to compare the efficacy of immune checkpoint inhibitors in advanced non-small cell lung cancer (NSCLC) patients with liver metastases.

Materials And Methods: English literature was retrieved from the PubMed, American Society of Clinical Oncology, and European Society for Medical Oncology databases from January 2015 to January 2021. We pooled the overall survival (OS) and progression-free survival (PFS) hazard ratios (HRs) using an NMA and ranked treatments by the surface under the cumulative ranking curve.

Autophagy is Involved in Neuroprotective Effect of Alpha7 Nicotinic Acetylcholine Receptor on Ischemic Stroke.

The α7 nicotinic acetylcholine receptor (α7nAChR) belongs to the superfamily of cys loop cationic ligand-gated channels, which consists of homogeneous α7 subunits. Although our lab found that activation of α7nAChR could alleviate ischemic stroke, the mechanism is still unknown. Herein, we explored whether autophagy is involved in the neuroprotective effect mediated by α7nAChR in ischemic stroke.

Toxicological and physiological effects of successive exposure to ochratoxin A at food regulatory limits.

Ochratoxin A (OTA), a potent mycotoxin, is a common contaminant of agro-products, which seriously threatens food safety. The OTA regulatory limits vary from different countries/regions. However, little is known about the toxicological effects of successive exposure to regulatory levels of OTA.

Protein Kinase Inhibitor Peptide as a Tool to Specifically Inhibit Protein Kinase A.

The protein kinase enzyme family plays a pivotal role in almost every aspect of cellular function, including cellular metabolism, division, proliferation, transcription, movement, and survival. Protein kinase A (PKA), whose activation is triggered by cyclic adenosine monophosphate (cAMP), is widely distributed in various systems and tissues throughout the body and highly related to pathogenesis and progression of various kinds of diseases. The inhibition of PKA activation is essential for the study of PKA functions.

Preparation of Quaternary Ammonium Salt-Modified Chitosan Microspheres and Their Application in Dyeing Wastewater Treatment.

An efficient adsorbent (a quaternary ammonium salt-modified chitosan microsphere, CTA-CSM) was synthesized via an emulsion cross-linking reaction between 3-chloro-2-hydroxypropyl trimethyl ammonium chloride (CTA) and chitosan (CS). The adsorption efficiency of the CTA-CSM as an adsorbent was studied using methyl orange dye to evaluate its suitability for wastewater purification. The characterization results showed that the CTA groups were successfully grafted onto the CS microspheres, and the as-prepared CTA-CSM samples exhibited a smooth surface and good dispersibility.

Synthesis and characterization of magnetic chitosan microspheres for drug delivery.

A novel magnetic microsphere was prepared by simple microemulsion polymerization for protein drug delivery systems. The FeO magnetic nanoparticles were successfully encapsulated in chitosan microspheres, which endowed the chitosan microspheres with good magnetism. The drug loading performance results indicated that the prepared magnetic chitosan microspheres exhibited a superior drug loading capacity, and the drug loading amount reached 947.

Activating α7 nicotinic acetylcholine receptor inhibits NLRP3 inflammasome through regulation of β-arrestin-1.

Aims: To evaluate whether activating α7 nicotinic acetylcholine receptor (α7nAChR) could inhibit the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome through regulation of β-arrestin-1 in monocyte/macrophage system, thus contributing to the control of neuroinflammation.

Methods: The protein levels of NLRP3, caspase-1 (Casp-1) p20 and proCasp-1, interleukin-1β (IL-1β) p17 and proIL-1β, IL-18 and proIL-18 were measured using Western blotting. The mRNA levels of Casp-1 and IL-1β were detected by real-time PCR (RT-PCR).

Autophagy Plays an Important Role in Anti-inflammatory Mechanisms Stimulated by Alpha7 Nicotinic Acetylcholine Receptor.

Alpha7 nicotinic acetylcholine receptor (α7nAChR) has been reported to alleviate neuroinflammation. Here, we aimed to determine the role of autophagy in α7nAChR-mediated inhibition of neuroinflammation and its underlying mechanism. Experimental autoimmune encephalomyelitis (EAE) mice and lipopolysaccharide-stimulated BV2 microglia were used as and models of neuroinflammation, respectively.

Intestinal Autophagy and Its Pharmacological Control in Inflammatory Bowel Disease.

Intestinal mucosal barrier, mainly composed of the intestinal mucus layer and the epithelium, plays a critical role in nutrient absorption as well as protection from pathogenic microorganisms. It is widely acknowledged that the damage of intestinal mucosal barrier or the disturbance of microorganism balance in the intestinal tract contributes greatly to the pathogenesis and progression of inflammatory bowel disease (IBD), which mainly includes Crohn's disease and ulcerative colitis. Autophagy is an evolutionarily conserved catabolic process that involves degradation of protein aggregates and damaged organelles for recycling.

Combined administration of anisodamine and neostigmine rescued acute lethal crush syndrome through α7nAChR-dependent JAK2-STAT3 signaling.

Previously we showed that Ani (anisodamine)/Neo (neostigmine) combination produced anti-shock effect via activating α7 nicotinic acetylcholine receptor (α7nAChR). In this study, we aim to investigate the therapeutic effect and underlying mechanisms of Ani/Neo combination in acute lethal crush syndrome (CS). In rat and rabbit CS models, Ani/Neo combination increased the 24 h survival rates, improved hemodynamics and decreased the levels of creatine kinase, MB isoenzyme of creatine kinase, blood urea nitrogen, creatinine, K in serum.

Activation of Cannabinoid Receptor 2 Ameliorates DSS-Induced Colitis through Inhibiting NLRP3 Inflammasome in Macrophages.

Activation of cannabinoid receptor 2 (CB2R) ameliorates inflammation, but the underlying mechanism remains unclear. In the present study, we examined whether activation of CB2R could suppress the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome. In peritoneal macrophages isolated from C57BL/6 mice, LPS/DSS challenge for 24 h increased the expression of the components of NLRP3 inflammasome NLRP3, Casp-1 p20/Casp-1 p45 ratio, proIL-1β and IL-1β and also enhanced autophagy (LC3-II/LC3-I ratio, Beclin-1 and SQSTM1).

Activating cannabinoid receptor 2 alleviates pathogenesis of experimental autoimmune encephalomyelitis via activation of autophagy and inhibiting NLRP3 inflammasome.

Aims: Activation of cannabinoid receptor 2 (CB2R) has been reported to ameliorate the pathogenesis of experimental autoimmune encephalomyelitis (EAE). In this study, we examined whether autophagy is involved in the beneficial effect of CB2R on EAE and explored the mechanism with a focus on inflammasome activation.

Methods: EAE severity was analyzed with clinical score and histological score stained by hematoxylin and eosin or luxol fast blue in spinal cord.

The protective action of ketanserin against lipopolysaccharide-induced shock in mice is mediated by inhibiting inducible NO synthase expression via the MEK/ERK pathway.

Nitric oxide (NO) plays an important role in the pathogenesis of endotoxic shock. This work tested the hypothesis that ketanserin could attenuate endotoxic shock by inhibiting the expression of inducible NO synthase (iNOS). The results demonstrated that ketanserin could inhibit iNOS expression in the heart, lungs, liver, and kidneys and nitrate production in the serum upon endotoxic shock in mice.