IPL treatment improves the symptom score of patients, associated ocular-surface indexes, MG function, and MG macrostructure as well as eyelid hygiene. And IPL treatment particularly improves MG microstructure and decreases MG inflammation in MGD patients.
The aim of this study was to evaluate the wound healing of adipose-derived stem cells (ADSCs) seeded on electrospinning poly (L-lactide-co-ε-caprolactone)/poloxamer (PLCL/P123) scaffolds and the mechanisms using a rat skin tissue injury model. CM-Dil labeled ADSCs were seeded on PLCL/P123 scaffolds for 48 h (ADSCs- PLCL/P123). Twelve Sprague-Dawley rats were randomly divided into three groups: ADSCs-PLCL/P123 (A group); PLCL/P123 alone (B group); petrolatum gauze (C group). Two 1.5 cm diameter circular impressions were made by placement of a punch biopsy instrument. The wound closure percentages were calculated by planimetry on postoperative day 0, 3, 12 and 21. On postoperative day 21, full-thickness skins from each group were examined by H&E staining, CK10 and CD31 immunohistochemical staining, and CK10 immunofluorescence staining respectively. The wound closure percentages on postoperative day 21 in A, B and C groups were 95.7% ± 3.9%, 83.2% ± 15.4% and 64.3% ± 6.2%, respectively (p < 0.05). H&E staining and immunohistochemical staining showed that the epidermal structure of A group was complete and possessed the characteristics of epidermal cells, and the CK10 staining positive suggested that ADSCs were differentiated into epidermal-like structures. The microvessel density of A group was significantly higher than that of the B and C groups (p < 0.05), while no significant differences were observed between B group and C group (p > 0.05). The ADSCs seeded on PLCL/P123 scaffolds could promote wound healing and have the potential to become a new therapeutic alternative material for skin tissue engineering.
Background and Aims:The effect of ginsenoside Rb1 on D-galactosamine (D-GalN)/lipopolysaccharide (LPS)-induced acute liver injury (ALI) is unknown. The aim of this study was to evaluate the effect of ginsenoside Rb1 on ALI and its underlying mechanisms. Methods: Mice were pretreated with ginsenoside Rb1 by intraperitoneal injection for 3 days before D-GalN/LPS treatment, to induce ALI. The survival rate was monitored every hour for 24 h, and serum biochemical parameters, hepatic index and histopathological analysis were evaluated to measure the degree of liver injury. ELISA was used to detect oxidative stress and inflammatory cytokines in hepatic tissue and serum. Immunohistochemistry staining, RT-PCR and western blotting were performed to evaluate the expression of toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), and NLR family, pyrin domain-containing 3 protein (NLRP3) in liver tissue and Kupffer cells (KCs). Results: Ginsenoside Rb1 improved survival with D-GalN/LPS-induced ALI by up to 80%, significantly ameliorated the increased alanine and aspartate transaminase, restored the hepatic pathological changes and reduced the levels of oxidative stress and inflammatory cytokines altered by D-GalN/LPS. Compared to the control group, the KCs were increased in the D-GalN/ LPS groups but did not increase significantly with Rb1 pretreatment. D-GalN/LPS could upregulate while Rb1 pretreatment could downregulate the expression of interleukin (IL)-1β, IL-18, NLRP3, apoptosis associated speck-like protein containing CARD (ASC) and caspase-1 in isolated KCs. Furthermore, ginsenoside Rb1 inhibited activation of the TLR4/NF-κB signaling pathway and NLRP3 inflammasome induced by D-GalN/LPS administration. Conclusions: Ginsenoside Rb1 protects mice against D-GalN/LPS-induced ALI by attenuating oxidative stress and the inflammatory response through the TLR4/NF-κB signaling pathway and NLRP3 inflammasome activation.
Keloid is a kind of pathological skin scar with unclear molecular pathology. Circular RNAs (circRNAs) are involved in the occurrence and development of many diseases; however, their relationship with keloid is not well understood. To investigate the involvement of dysregulated circRNAs in keloid. Thirty-seven keloids and 37 normal skin tissues were collected, and the changes of circRNAs, microRNAs (miRNAs) and mRNAs in 3 keloids and 3 normal samples by high-throughput sequencing were detected first. Based on the circRNA-miRNA-mRNA interaction network construction, gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis combining several signaling pathways associated with keloid formation and progression, the circRNAs required further verification were screened out. The expression levels of the selected circRNAs were verified in 37 keloids and 37 normal skin tissues using quantitative real-time polymerase chain reaction (QPCR). The interaction of candidate circRNA and its predicted binding miRNA was tested by dualluciferase reporter gene experiment. Compared with normal controls, there was an average of 120 and 12 circRNAs, 44 and 63 miRNAs, 656 and 156 mRNAs were upregulated and downregulated, respectively, in keloids. According to the analysis of bioinformation, six circRNAs were picked out. The QPCR validation results of two upregulated circRNAs (hsa_circ_0001320 and circCOL5A1) were consistent with previous sequencing results. The interaction between hsa_circ_0001320 and miR-574-5p was confirmed. This study makes it clear that the abnormal expression of cir-cRNAs may be related to the pathological process of keloid.
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