Gut microbiome plays a vital role in post-stroke injury repair by mediating neuroinflammation.

Cerebral stroke is a common neurological disease and often causes severe neurological deficits. With high morbidity, mortality, and disability rates, stroke threatens patients' life quality and brings a heavy economic burden on society. Ischemic cerebral lesions incur pathological changes as well as spontaneous nerve repair following stroke. Strategies such as drug therapy, physical therapy, and surgical treatment, can ameliorate blood and oxygen supply in the brain, hamper the inflammatory responses and maintain the structural and functional integrity of the brain. The gut microbiome, referred to as the "second genome" of the human body, participates in the regulation of multiple physiological functions including metabolism, digestion, inflammation, and immunity. The gut microbiome is not only inextricably associated with dangerous factors pertaining to stroke, including high blood pressure, diabetes, obesity, and atherosclerosis, but also influences stroke occurrence and prognosis. AMPK functions as a hub of metabolic control and is responsible for the regulation of metabolic events under physiological and pathological conditions. The AMPK mediators have been found to exert dual roles in regulating gut microbiota and neuroinflammation/neuronal apoptosis in stroke. In this study, we reviewed the role of the gut microbiome in cerebral stroke and the underlying mechanism of the AMPK signaling pathway in stroke. AMPK mediators in nerve repair and the regulation of intestinal microbial balance were also summarized.

MiR-203a-3p/153-3p improves cognitive impairments induced by ischemia/reperfusion via blockade of SRC-mediated MAPK signaling pathway in ischemic stroke.

Stroke is a leading cause of death and disability worldwide and the cerebral ischemia/reperfusion (I/R) induced injury is a common phenomenon of stroke. The pathogenesis and effective treatment of I/R-induced brain tissue damage is limited. In this study, the rat model of middle cerebral artery occlusion (MCAO) and the cell model of oxygen and glucose deprivation/reperfusion (OGD/R) were applied to investigate the possible role of the microRNA in ischemic stroke. MCAO/R and OGD/R caused the downregulation of miR-203a-3p and miR-153-3p, the upregulation of SRC. SRC was identified to be a common target for miR-203a-3p and miR-153-3p. Both miR-203a-3p and miR-153-3p inhibited SRC expression at the mRNA and protein levels. miR-203a-3p and miR-153-3p improved the cognitive deficits through targeting SRC. Moreover, miR-203a-3p and miR-153-3p relieved the apoptosis, decreases NLRP3 inflammasome activity, decreases oxidative stress and inflammation in hippocampal neuron through targeting SRC. Moreover, the MAPK signaling pathway was confirmed to be the downstream for miR-203a-3p and miR-153-3p in vivo and in vitro. Thus, miR-203a-3p and miR-153-3p confers neuroprotective effects against ischemic stroke via attenuation of apoptosis, oxidative stress and inflammatory pathways through inhibiting SRC-dependent MAPK signaling pathway in vivo and in vitro, suggesting new therapeutic targets for the prevention and treatment of stroke.

miR-185-5p alleviates CCI-induced neuropathic pain by repressing NLRP3 inflammasome through dual targeting MyD88 and CXCR4.

MicroRNAs (miRNAs) are important modulators in the evolvement and progression of neuropathic pain (NP). According to reports, miR-185-5p contributes to various diseases and inflammatory responses. However, it is not clear whether miR-185-5p mediates neuroinflammation and NP following chronic constrictive injury (CCI). The CCI model was constructed in rats to induce NP. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were employed to evaluate pain threshold in CCI rats. The expression of miR-185-5p, GFAP, Iba1, Caspase-3-positive cells, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL)-labeled apoptotic neurons, inflammatory mediators, including interleukin (IL)-6, IL-1ß and tumor necrosis factor-α (TNF-α) in lumbar portion (L4-L6) of CCI rats were determined. Furthermore, the targets of miR-185-5p were predicted by the Starbase, and the binding association between miR-185-5p and MyD88, miR-185-5p and CXCR4 was verified by the dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. As shown by the data, miR-185-5p was distinctly reduced in L4-L6 spinal cord tissues of rats after CCI. Up-regulating miR-185-5p alleviated mechanical and thermal hyperalgesia, inactivated microglia and astrocytes accumulation, and abated the contents of IL-1ß, IL-6 and TNF-α in L4-L6 spinal cord tissues of CCI rats. Bioinformatics analysis suggested that MyD88 and CXCR4 were potential target genes of miR-185-5p. Increasing miR-185-5p expression notably impeded the expression of MyD88, CXCR4 and NLRP3 inflammasome in BV2 microglia, while attenuating miR-185-5p expression exerted the opposite effects. Notably, down-regulating MyD88 and CXCR4 significantly enhanced the miR-185-5p-mediated anti-inflammatory effects, and reversed miR-185-5p inhibitor-mediated proinflammatory effects. Additionally, up-regulating miR-185-5p repressed BV2-induced neuronal apoptosis and increased neuronal viability. In conclusion, this study suggested that miR-185-5p chokes CCI-induced NP and neuroinflammation by targeting MyD88 and CXCR4, indicating that miR-186-5p is an underlying therapeutic target for NP.

A Review of Processes for Removing Antibiotics from Breeding Wastewater.

Antibiotic pollution has become an increasingly serious issue due to the extensive application of antibiotics, their resistance to removal, and the harmful effects on aquatic environments and humans. Breeding wastewater is one of the most important sources of antibiotics in the aquatic environment because of the undeveloped treatment systems in breeding farms. It is imperative to establish an effective antibiotic removal process for breeding wastewater. This paper reviews the treatment methods used to remove antibiotics from breeding wastewater. The mechanisms and removal efficiency of constructed wetlands, biological treatments, advanced oxidation processes (AOPs), membrane technology, and combined treatments are explained in detail, and the advantages and disadvantages of the various treatment methods are compared and analyzed. Constructed wetlands have high removal rates for sulfonamide (SM), tetracycline (TC), and quinolone (QN). The antibiotic removal efficiency of biological treatment methods is affected by various processes and environmental factors, whereas AOPs and combined treatment methods have better antibiotic removal effects. Although it has broad application prospects, the application of membrane technology for the treatment of antibiotics in breeding wastewater needs further research.

Cooperation of Fe(II) and peroxymonosulfate for enhancement of sulfamethoxazole photodegradation: mechanism study and toxicity elimination.

This study aims at systematically examining the potential of removing the emerging pollutant sulfamethoxazole (SMX) from aqueous solution under photo-assisted peroxymonosulfate (PMS) activation by Fe(ii). The residual SMX was determined by HPLC analysis. The concentration of Fe(ii) ([Fe(ii)]) was monitored during SMX degradation. Fe(ii) and PMS cooperated with each other for faster SMX photodegradation; a relatively lower or higher molar ratio between Fe(ii) and PMS led to lower SMX removal efficiency due to the insufficient radicals or scavenging effect. A fixed reaction ratio of [Fe(ii)]Δ : [PMS]0 with 1.6 : 1 at the first 5 min was detected for reactions with [Fe(ii)]0 ≥ 0.5 mM or [PMS]0 ≤ 0.25 mM. The pH level of around 6.0 was recommended for optimal SMX removal under the treatment process UVA + Fe(ii) + PMS. Six transformation products were detected through UPLC/ESI-MS analysis, and four of the proposed intermediates were newly reported. Concentrations of the intermediates were proposed based on the isoxazole-ring balance and the Beer-Lambert law. Total Organic Carbon (TOC) reduction was mainly attributed to the loss of benzene ring, N-S cleavage, and isoxazole ring opening during SMX degradation. The contributions of reactive species OH˙ and SO4˙- were determined based on quench tests. The acute toxicity of SMX to the rotifers was eliminated after the proposed treatment, demonstrating that the process was effective for SMX treatment and safe to the environment.