Proparacaine Hydrochloride

This umbrella review aimed to determine the various drugs used to treat trigeminal neuralgia (TN) and to evaluate their efficacies as well as side effects by surveying previously published reviews. An online search was conducted using PubMed, CRD, EBSCO, Web of Science, Scopus, and the Cochrane Library with no limits on publication date or patients' gender, age, and ethnicity. Reviews and meta-analyses of randomized controlled trials pertaining to drug therapy for TN, and other relevant review articles added from their reference lists, were evaluated. Rapid reviews, reviews published in languages other than English, and reviews of laboratory studies, case reports, and series were excluded. A total of 588 articles were initially collected; 127 full-text articles were evaluated after removing the duplicates and screening the titles and abstracts, and 11 articles were finally included in this study. Except for carbamazepine, most of the drugs had been inadequately studied. Carbamazepine and oxcarbazepine continue to be the first choice for medication for classical TN. Lamotrigine and baclofen can be regarded as second-line drugs to treat patients not responding to first-line medication or for patients having intolerable side effects from carbamazepine. Drug combinations using carbamazepine, baclofen, gabapentin, ropivacaine, tizanidine, and pimozide can yield satisfactory results and improve the tolerance to the treatment. Intravenous lidocaine can be used to treat acute exaggerations and botulinum toxin-A can be used in refractory cases. Proparacaine, dextromethorphan, and tocainide were reported to be inappropriate for treating TN. Anticonvulsants are successful in managing trigeminal neuralgia; nevertheless, there have been few studies with high levels of proof, making it challenging to compare or even combine their results in a statistically useful way. New research on other drugs, combination therapies, and newer formulations, such as vixotrigine, is awaited. There is conclusive evidence for the efficacy of pharmacological drugs in the treatment of TN.

The corneal endothelium is a monolayer, which mediates solute and water flux across the posterior corneal surface. Alcaine's main component proparacaine is paramount in human corneal endothelium (HCE) cell regulation. This study explored the mechanism of alcaine in regulating HCE cells. HCE cell morphology under gradient concentrations was observed by an optical microscope. Cell proliferation and viability were detected by MTT assay to determine the half inhibitory concentration (IC 50). Cell apoptosis rate, HIF-1α mRNA expression, and HIF-1α, p/t-JNK and Caspase-3 protein levels were detected by flow cytometry, RT-qPCR, and Western blot. After treatment with alcaine at 0.625-5 g/L concentration range for 24 h, HCE cells showed cytoplasmic vacuolation, cell shrinkage, separation from culture matrix, and eventual death. Alcaine treated-HCE cell proliferation was decreased in a dose-dependent manner. The IC 50 of alcaine was 1.26 g/L. After alcaine treatment, HCE cell apoptosis rate was promoted and HIF-1α levels in HCE cells were stimulated. Knockdown of HIF-1α partially annulled the effects of alcaine on inhibiting HCE cell proliferation and facilitating apoptosis. Alcaine might activate the JNK/caspase-3 pathway by increasing HIF-1α. The inhibition of the JNK/caspase-3 pathway partially abrogated the effects of alcaine on inhibiting HCE cell proliferation and promoting apoptosis. Alcaine might affect HCE cell proliferation and apoptosis by upregulating HIF-1α and activating the JNK/caspase-3 pathway.