Therapeutic application of decellularized porcine small intestinal submucosa scaffold in conjunctiva reconstruction.

The objective of this study was to investigate the biological feasibility and surgical applicability of decellularized porcine small intestinal submucosa (DSIS) in conjunctiva reconstruction. A total of 52 Balb/c mice were included in the study. We obtained the DSIS by decellularization, evaluated the physical and biological properties of DSIS in vitro, and further evaluated the effect of surgical transplantation of DSIS scaffold in vivo. The histopathology and ultrastructural analysis results showed that the scaffold retained the integrity of the fibrous morphology while removing cells. Biomechanical analysis showed that the elongation at break of the DSIS (239.00 ± 12.51%) were better than that of natural mouse conjunctiva (170.70 ± 9.41%, P < 0.05). Moreover, in vivo experiments confirmed the excellent biocompatibility of the decellularized scaffolds. In the DSIS group, partial epithelialization occurred at day-3 after operation, and the conjunctival injury healed at day-7, which was significantly faster than that in human amniotic membrane (AM) and sham surgery (SHAM) group (P < 0.05). The number and distribution of goblet cells of transplanted DSIS were significantly better than those of the AM and SHAM groups. Consequently, the DSIS scaffold shows excellent biological characteristics and surgical applicability in the mouse conjunctival defect model, and DSIS is expected to be an alternative scaffold for conjunctival reconstruction.

The role of regulated necrosis in inflammation and ocular surface diseases.

In recent decades, numerous types of regulated cell death have been identified, including pyroptosis, ferroptosis and necroptosis. Regulated necrosis is characterized by a series of amplified inflammatory responses that result in cell death. Therefore, it has been suggested to play an essential role in the pathogenesis of ocular surface diseases. The cell morphological features and molecular mechanisms of regulated necrosis are discussed in this review. Furthermore, it summarizes the role of ocular surface diseases, such as dry eye, keratitis, and cornea alkali burn, as potential disease prevention and treatment targets.

Association between poor sleep quality and an increased risk of dry eye disease in patients with obstructive sleep apnea syndrome.

Purpose: Obstructive sleep apnea (OSA) is related to an increased incidence of dry eye disease (DED). However, their exact relationship is unknown and requires further well-designed studies with advanced mechanisms detection. Patients and methods: This case-control study included 125 OSA cases and 125 age-gender-matched controls enrolled in the hospital between 1 January and 1 October 2021. OSA diagnosis and classification were performed using a polysomnography (PSG) assay. Detailed ophthalmological examinations, including the Schirmer I test, corneal staining, and ocular surface disease index (OSDI), were used to detect DED-related parameters. A comprehensive ocular surface assay was performed to measure a series of parameters, including first non-invasive first tear film break-up time (f-NIBUT), average non-invasive first tear film break-up time (av-NIBUT), tear meniscus height (TMH), and loss of meibomian gland. In addition, the Pittsburgh Sleep Quality Index (PSQI) scale was used to assess sleep quality. Results: Compared to the control, the OSA group showed an increased DED risk (P = 0.016) along with an increased PSQI score and a higher rate of poor quality sleep (P < 0.001 and P = 0.007, respectively). Stratification of OSA cases indicated that DED-related parameters were impaired in patients with severe OSA (P < 0.05). The analysis of DED-parameters-related factors showed significant correlations between OSA-related indexes and PSQI (P < 0.05). Moreover, the poor sleep quality group in the OSA cases showed worse DED-related parameters (P < 0.05), which was not observed in the control group. Conclusion: OSA, especially the severe stage OSA, was related to an increased risk of DED. Also, sleep quality was correlated with the onset of both OSA and DED, where poor sleep quality revealed a relationship between OSA and the risk of DED. Overall, our findings provided evidence for advanced management of DED and OSA in future.

Nicotinamide mononucleotide increases cell viability and restores tight junctions in high-glucose-treated human corneal epithelial cells via the SIRT1/Nrf2/HO-1 pathway.

BACKGROUND: Diabetes mellitus (DM)-related corneal epithelial dysfunction is a severe ocular disorder; however, the effects of nicotinamide mononucleotide (NMN) on high-glucose (HG)-treated human corneal epithelial cells (HCECs) remain unclear. METHODS: We conducted an in-vitro study to examine the effects of NMN treatment on HG-treated HCECs. Cell viability was measured using trypan blue stain, mitochondrial membrane potential was measured using JC-1 stain, and intracellular reactive oxygen species and apoptosis assays were conducted using flow cytometry. Transepithelial electrical resistance (TEER) and zonula occludens-1 (ZO-1) immunofluorescence for tight junction examinations were conducted. Immunoblot analyses were conducted to analyze the expression of silent information regulator-1 (SIRT1), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) of the SIRT1/Nrf2/HO-1 pathway. RESULTS: NMN increased cell viability by reducing cell damage, reducing apoptosis, increasing cell migration, and restoring tight junctions in HG-treated HCECs. By analyzing the expressions of SIRT1, Nrf2, HO-1, NMN demonstrated protective effects via the SIRT1/Nrf2/HO-1 pathway. CONCLUSIONS: NMN increases cell viability by reversing cell damage, reducing apoptosis, increasing cell migration, and restoring tight junctions in HG-treated HCECs, and these effects may be mediated by the SIRT1/Nrf2/HO-1 pathway.