Mitochondria release many damage-associated molecular patterns (DAMPs) when cells are damaged or stressed, with mitochondrial DNA (mtDNA) being. MtDNA activates innate immune responses and induces inflammation through the TLR-9, NLRP3 inflammasome, and cGAS-STING signaling pathways. Released inflammatory factors cause damage to intestinal barrier function. Many bacteria and endotoxins migrate to the circulatory system and lymphatic system, leading to systemic inflammatory response syndrome (SIRS) and even damaging the function of multiple organs throughout the body. This process may ultimately lead to multiple organ dysfunction syndrome (MODS). Recent studies have shown that various factors, such as the release of mtDNA and the massive infiltration of inflammatory factors, can cause intestinal ischemia/reperfusion (I/R) injury. This destroys intestinal barrier function, induces an inflammatory storm, leads to SIRS, increases the vulnerability of organs, and develops into MODS. Mitophagy eliminates dysfunctional mitochondria to maintain cellular homeostasis. This review discusses mtDNA release during the pathogenesis of intestinal I/R and summarizes methods for the prevention or treatment of intestinal I/R. We also discuss the effects of inflammation and increased intestinal barrier permeability on drugs.
Anti-β 2 -glycoprotein I (anti-β 2 GPI) is an anti-phospholipid antibody that specifically binds to β 2 GPI. There is growing evidence that this autoantibody is closely linked to specific thrombotic conditions. Cerebral infarction (CI) is a form of thrombosis associated with high rates of morbidity and mortality. In the present study, it was determined that patients with CI exhibited significantly increased serum anti-β 2 GPI levels as well as increased NLR family pyrin domain containing 3 (NLRP3) expression within neutrophils, suggesting a potential role for inflammatory cell death in this pathological context. Specifically, it was determined that anti-β 2 GPI/β 2 GPI is able to induce neutrophil pyroptosis, thereby driving these cells to release IL-1β via a pathway regulated by cell surface Toll-like receptor 4 expression. At the mechanistic level, the double-stranded RNA-dependent protein kinase/p38MAPK/NLRP3 pathway was indicated to govern anti-β 2 GPI/β 2 GPI-induced neutrophil pyroptosis. These pyroptotic neutrophils were also observed to release large amounts of high mobility group box protein 1, which, together with IL-1β, promoted IL-8 and intercellular cell adhesion molecule-1 upregulation in endothelial cells. In summary, these data suggest that inhibiting neutrophil pyroptosis may represent a viable approach to treating anti-β 2 GPI antibody-associated cI.
Background We aimed to evaluate the long-term clinical outcomes of Toric intraocular lens (Toric IOL)and Acrysof IQ Restor Toric +3.0D intraocular lens (ART +3.0D IOL)in patients with cataract and corneal astigmatism.Methods Fifty-eight eyes (46 participants) that had Toric IOL implantation, forty-three eyes (31 participants) that had ART +3.0D IOL implantation, were included in the study. All participants were assessed preoperatively, 3, 6, 12 and 24 months postoperatively. Primary outcomes measure: uncorrected distance visual activity (UCDVA), uncorrected near visual acuity (UCNVA), astigmatism and IOL axis alignment, defocus curve, contrast sensitivity and ocular aberration.Results UCDVA was better than 0.3 LogMAR at 3, 6, 12 and 24 months after surgery in both groups, and UCDVA was significantly improved after surgery than before ( P <0.05). All patients with ART +3.0D IOL implanted after surgery achieved or exceeded the near-vision of Jr3, which could meet the needs for removal of lens. At 3, 6, 12 and 24 months after surgery, the residual astigmatic was (0.28±0.20) diopters(D), (0.32±0.25) D, (0.31±0.16) D, (0.32±0.22) D in Toric group, and (0.27±0.17) D, (0.31±0.21) D, (0.30±0.19) D, (0.33±0.20) D respectively in the ATR group. Compared with preoperative corneal astigmatism, the difference was statistically significant ( P <0.05). The IOL axial mobility of all the patients was less than 5°in the two groups within 2 years after the operation. There was no difference in aberrations between the ART group and the Toric group under 3mm pupil, and there was statistically significant difference between the ART group and the Toric group under 5mm pupil ( P <0.05).Conclusions Toric IOL and ART + 3.0D IOL implantation were safe and effective in the treatment of cataract with corneal astigmatism,and ART + 3.0D IOL provided adequate near vision. The effect had long-term stability.
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