Inhibition of poly (ADP-ribose) polymerase 1 in neuron cells might enhance the therapeutic effect of leonurine under cholesterol stimulation.

Atherosclerosis (AS) is a chronic inflammatory disease with high morbidity and mortality worldwide and is the pathologic basis of cerebral-cardiovascular disease. Cerebral infarction is caused by cerebral ischemia in the deep brain stem or cerebral hemisphere, and small vessel atherosclerosis is the pathophysiological basis of lacunar cerebral infarction. In this study, we found that inhibition of PARP1 in neuronal cells increased the proliferation rate of cells, reduced the concentration of cholesterol in neuronal cells, inhibited the expression and secretion of proinflammatory factors and promoted the expression and secretion of proangiogenic factors. In addition, the reverse transport process of cholesterol and autophagy process were activated in neuron cells by detecting the target proteins using western blotting analysis, and further experiments found that this process might be mediated by activation of the PI3K/AKT/mTOR signalling pathway. Thus, we thought inhibition of PARP1 might be a new therapeutic method for cerebral-cardiovascular disease.

MiR-125a-5p Alleviates Dysfunction and Inflammation of Pentylenetetrazol- induced Epilepsy Through Targeting Calmodulin-dependent Protein Kinase IV (CAMK4).

BACKGROUND: MicroRNAs (miRNA) are known to play a key role in the etiology and treatment of epilepsy through controlling the expression of gene. However, miR-125a-5p in the epilepsy is little known. Epilepsy in rat models was induced by Pentylenetetrazol (PTZ) and miR- 125a-5p profiles in the hippocampus were investigated in our experiment. Also, the relationship between miR-125a-5p and calmodulin-dependent protein kinase IV (CAMK4) was identified and the related mechanism was also illustrated. METHODS: The miR-125a-5p mRNA expression levels were evaluated by quantitative real time polymerase chain reaction (qRT-PCR). Western Blot (WB) was used to analyze the CAMK4 protein expression levels. Seizure score, latency and duration were determined based on a Racine scale. The enzyme-linked immunosorbent assay (ELISA) was used to analyze the inflammatory factor expression. The relationship between miR-125a-5p and CAMK4 was detected through dual luciferase assay. RESULTS: Downregulation of miR-125a-5p was observed in the hippocampus of PTZ-induced epilepsy rats. The overexpression of miR-125a-5p attenuated seizure and decreased inflammatory factor level in the hippocampus of PTZ-induced rats. The miR-125a-5p alleviated epileptic seizure and inflammation in PTZ-induced rats by suppressing its target gene, CAMK4. CONCLUSION: miR-125a-5p may represent a novel therapeutic treatment for PTZ-induced epilepsy by preventing the activation of CAMK4.