Abstract. The aim of the present study was to determine whether chlorogenic acid (CA) is able to modulate cadmium (Cd)-induced oxidative brain damage. Cd-treated rats displayed numerous pathological effects, including the inhibition of acetylcholinesterase, elevated lipid peroxidation, the depletion of enzymatic and non-enzymatic antioxidants, the reduction of membrane-bound ATPase activity, mitochondrial dysfunction and DNA fragmentation. Pretreatment of the rats with CA significantly attenuated these effects. These results lead to the hypothesis that the mechanisms by which CA attenuates the effects of Cd-induced oxidative brain damage include the maintenance of antioxidant homeostasis, inhibition of the membrane effects and the perpetuation of mitochondrial dysfunction. These data support the potential of CA as a beneficial intervention in the prevention of heavy metal poisoning due to Cd exposure.
Inflammatory response plays an important role in the pathogenesis of ischemic stroke and anti-inflammatory agents may provide a choice of treatment. Triptolide is reported to be anti-inflammatory. In this study, we investigated the effects of triptolide on cultured neuronal cell line in vitro and experimental ischemic stroke in vivo. Oxygen-glucose deprivation (OGD) and tumor necrosis factor-α (TNF-α) stimulated SH-SY5Y cells were incubated with triptolide. In vivo, rats were subjected to middle cerebral artery occlusion (MCAO) for 1 h, followed by reperfusion for 23 h. Results of this study showed that triptolide treatment reduced the OGD-induced cytotoxicity and apoptosis and blocked TNF-α-induced activation of NF-κB and p38MAPK in SH-SY5Y cells. Intraperitoneal injection of triptolide showed significant neuroprotective actions in stroke rats. Triptolide attenuated neurological deficit, brain infarct volume, and brain water content, and inhibited activation of NF-κB and p38MAPK. These data show that triptolide protects rats against ischemic cerebral injury via inhibiting NF-κB and p38MAPK signaling pathways.
Glioma is the most aggressive tumor of the central nervous system. Long non-coding RNAs (lncRNAs) may be involved in modulating tumor generation. The present study analyzed an lncRNA microarray of glioma and selected long intergenic non-protein coding RNA 665 ( LINC00665 ) as the research object. The mode of expression and biological function of LINC00665 in glioma were assessed using lncRNA microarray and RT-qPCR analyses. Gain-of-function assays and/or loss-of-function assays were implemented to explore the role of LINC00665 in the progression of glioma. Dual-luciferase reporter and RNA immunoprecipitation assays explored the downstream molecular mechanism of LINC00665 . The function of the molecular pathway in progression of glioma was analyzed using rescue assays. High expression of LINC00665 was marked in glioma tissues and cells, which correlated with an unsatisfactory prognosis. Upregulation of LINC00665 significantly promoted the proliferation and invasion of glioma cells. LINC00665 acted as a competing endogenous RNA by sponging miR-34a-5p to upregulate angiotensin II receptor type 1 (AGTR1). LINC00665 promoted the progression of glioma by acting as a competitive endogenous RNA to competitively bind to miR-34a-5p and mediate AGTR1 expression.
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