Migraine is one of the most common neurological disorders which poses significant socioeconomic burden worldwide. Neuroinflammation and oxidative stress both play important roles in the pathogenesis of migraine. Human urinary kallidinogenase (UK) is a tissue kallikrein derived from human urine. Increasing evidence suggests that UK may protect against ischemic stroke, but UK’s treatment potential against migraine remains to be explored. Immortal BV-2 murine microglial cells were treated with UK (125 nM, 250 nM, and 500 nM) and then given lipopolysaccharides (LPS, 1000 ng/mL). Cell viability of BV-2 cells was tested by the CCK-8 assay. Expressions of tumor necrosis factor-α (TNFα), prostaglandin E2 (PGE2), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were examined with the ELISA method and western blot. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) were measured to determine oxidative stress. Our results showed that LPS administration increased the levels of proinflammatory cytokines (TNFα, PGE2, IL-6, and IL-1β) and oxidative stress (ROS and MDA) when compared with the control group and decreased significantly upon introduction with UK. Taken together, UK treatment reduced LPS-induced neuroinflammation and oxidative stress in a dose-dependent manner, which might be a potential treatment of migraine.
Stroke is the second leading cause of death and disability in the world, with a heavy burden on patients, their families, and society. At present, a major focus of cerebrovascular disease research is to find a safe and effective new method to promote early functional recovery in the acute phase of cerebral infarction. Major ozonated autohemotherapy (MOAH) can maintain ATP and energy metabolism in cerebral ischemia and hypoxia, and reduce cell apoptosis. In the current study, the model of middle cerebral artery occlusion in the Sprague Dawley rat was established and evaluated by the clinical functional score, Hoechst staining, immunohistochemistry, Western blot analysis, and biochemical detection. Then, the effects of MOAH on neurological function, apoptosis, and oxygen free radical damage after acute ischemia in middle cerebral artery were evaluated. Moreover, the potential two mechanisms have been illustrated for MOAH effects. This study would lay a theoretical foundation for the application of MOAH and find an effective and early treatment method for the cerebral infarction.
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