Background To determine the effect of sodium hyaluronate combined with recombinant human epidermal growth factor (rhEGF) on clinical symptoms and inflammation in patients with newly diagnosed xerophthalmia after cataract surgery. Methods A total of 106 patients who underwent cataract surgery and were newly diagnosed with xerophthalmia in our hospital between June 2018 and August 2019 were enrolled. Of these, 50 patients who were treated with sodium hyaluronate (0.1%) were assigned to the monotherapy group (MG) and the remaining 56 patients who were treated with sodium hyaluronate (0.1%) combined with rhEGF (20 μg/ml) were assigned to the combination group (CG). The 2 groups were compared based on ocular surface disease index (OSDI) score, break-up time (BUT), fluorescein corneal staining level, Schirmer I test (SI) level, clinical efficacy (disappearance of typical symptoms, including eyes drying, burning sensation, foreign body sensation, etc), and interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α) levels. Spearman correlation analysis was conducted to analyze the relationship between IL-1, IL-6, TNF-α and clinical efficacy. In addition, receiver operating characteristic curves were drawn to analyze the predictive value of IL-1, IL-6, and TNF-α in efficacy on xerophthalmia. Results: After treatment, the CG showed reduced OSDI score compared with the MG. The CG showed increased BUT (s) and SI (mm) levels compared with MG. After treatment, the CG exhibited decreased levels of IL-1(ng/mL), IL-6 (ng/mL), and TNF-α (ng/mL) compared with the MG. Spearman correlation analysis revealed that IL-1, IL-6, and TNF-α were negatively correlated with clinical efficacy. The areas under the curves of IL-1, IL-6, and TNF-α were 0.801, 0.800, and 0.736 respectively. Conclusions Sodium hyaluronate combined with rhEGF is helpful to alleviate clinical symptoms and inflammation in patients with xerophthalmia undergoing cataract surgery.
Globally, diabetes has assumed epidemic proportions with the neuropathic complications attributed to the malady emerging as a substantial burden on patients and society. DNP has greatly affected the daily life of patients, the effect of traditional treatment methods is not ideal, and it is easy to produce drug resistance. This work is aimed at scrutinizing the effect of upregulating the expression of TNFAIP3 on diabetic neuralgia in mice. This work entailed ascertaining the effects of TNFAIP3 on a murine DNP system. This inspired us to observe the analgesic effect via high expression of lentivirus-mediated TNFAIP3 by intrathecal injection in the animal model to explore its regulatory impacts, symptom relief, and mechanistic role in pain. The results displayed an attenuation of hind paw pain hypersensitivity by LV-TNFAIP3 in the animals. The spinal cord and dorsal root ganglion of mice with neuropathic pain displayed an evident dip in TNFAIP3. Inhibition of the ERK/NF-κB signaling pathway employing LV-TNFAIP3 conspicuously suppressed this pathway while the diabetic pain hypersensitivity was quelled. This effect was also seen with insulin treatment evidently. In conclusion, according to the above analyses, the interaction between DNP and extracellular signal-regulated kinase signal transduction pathway is one of the key factors of pathogenesis.
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