Zinc oxide nanoparticles ameliorate collagen lattice contraction in human tenon fibroblasts.

Glaucoma is a major cause of irreversible blindness in the world and filtering surgery is commonly carried out to control intraocular pressure. Failure of filtering surgery is usually due to postoperative scarring, and fibroblast proliferation, collagen production and subconjunctival fibrosis play a prominent role in obstructing aqueous humor from the anterior chamber to the subconjunctival space. Zinc oxide (ZnO) nanoparticles have been widely applied in biomedical fields.

Zinc oxide nanoparticles inhibit expression of manganese superoxide dismutase via amplification of oxidative stress, in murine photoreceptor cells.

Objectives: As a parenchymal cell, the photoreceptor is more susceptible to alterations in outer micro-environmental conditions than other cells. In the present study, we aimed to investigate inhibitory effects of zinc oxide (ZnO) nanoparticles on expression of manganese superoxide dismutase (MnSOD) in murine photoreceptor-derived cells.

Materials And Methods: We investigated effects of ZnO nanoparticles on murine photoreceptor cell viability and on expression and activity of MnSOD using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, immunofluorescence analysis, flow cytometry, quantitative real-time PCR and enzyme-linked immunosorbent assay (ELISA).

Effects of N-butylphthalide on the activation of Keap1/Nrf-2 signal pathway in rats after carbon monoxide poisoning.

Unlabelled: Carbon monoxide (CO) is the leading cause of death by poisoning all over the world and may result in neuropathologic changes and cognitive and neurologic sequelae, yet little is known regarding its outcomes. The present study aimed to evaluate the neuroprotective effects of N-butylphthalide (NBP) against brain damage after acute CO poisoning. The animal model of CO poisoning was established by exposed to 1000 ppm CO in air for 40 min and then to 3000 ppm for another 20 min.

Effects of N-Butylphthalide on the expressions of Nogo/NgR in rat brain tissue after carbon monoxide poisoning.

Carbon monoxide (CO) intoxication is one of the most common types of poisoning worldwide, and may result in neuropathologic sequelae, yet its pathogenesis is not clear and there is no optimal management strategy for patients with CO poisoning. In this study, the rat model of CO poisoning was established in a hyperbaric chamber by CO exposure. Rats were administered orally N-Butylphthalide (NBP) at a dose of 1 ml/100g.

Edaravone attenuates brain damage in rats after acute CO poisoning through inhibiting apoptosis and oxidative stress.

Acute carbon monoxide (CO) poisoning is the most common cause of death from poisoning all over the world and may result in neuropathologic and neurophysiologic changes. Acute brain damage and delayed encephalopathy are the most serious complication, yet their pathogenesis is poorly understood. The present study aimed to evaluate the neuroprotective effects of Edaravone against apoptosis and oxidative stress after acute CO poisoning.