Effect of poly-arginine R18 on neurocyte cell growth via autophagy in traumatic brain injury.

The present study assessed the effects of poly-arginine R18 and its promotion of neurocyte cell growth via autophagy in traumatic brain injury (TBI), and aimed to determine the possible mechanism by which this occurs. Brain water content was measured to analyze the effects of poly-arginine R18 in TBI. MTT and lactate dehydrogenase activity assays were performed to measure N2A cell growth. Western blotting and immunofluorescence staining were also performed to determine the protein expression of Bcl-2 associated X, LC3, Beclin-1 and p62. The results demonstrated that poly-arginine R18 treatment reduced neurocyte apoptosis and promoted neurocyte cell growth via the activation of autophagy in a rat model of TBI. Furthermore, poly-arginine R18 treatment promoted neurocyte cell growth, reduced apoptosis, induced the protein expression of LC3 and Beclin-1, and suppressed p62 expression by promoting autophagy in vitro. In addition, the inhibition of autophagy attenuated the effects of poly-arginine R18 on cell growth in vitro. Collectively, the results demonstrate the effects of poly-arginine R18 on neurocyte cell growth via autophagy activation in a model of TBI, and poly-arginine R18 is therefore a potential therapeutic target in TBI.

MicroRNA-145 inhibits the activation of the mTOR signaling pathway to suppress the proliferation and invasion of invasive pituitary adenoma cells by targeting AKT3 in vivo and in vitro.

PURPOSE: This study was designed to explore how miR-145 regulates the mTOR signaling pathway in invasive pituitary adenoma (IPA) by targeting AKT3. METHODS: A total of 71 cases of IPA tissues and 66 cases of non-IPA tissues were obtained in this study. In vitro, the IPA cells were assigned into blank control, empty plasmid, miR-145 mimic, miR-145 inhibitor, miR-145 mimic + rapamycin, miR-145 inhibitor + rapamycin and rapamycin groups. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were performed to detect the protein expressions of PI3K, AKT3, mTOR mRNA and the mRNA expression of miR-145 both in vivo and in vitro. Additionally, the S6K and RPS6 mRNA and protein expressions as well as the relative phosphorylation levels were determined in vitro. MTT assay, flow cytometry and transwell assay were used to testify the cell proliferation, apoptosis and invasion ability, respectively. RESULTS: The IPA tissues exhibited significantly lower expression of miR-145 but higher PI3K, AKT3 and mTOR mRNA and protein expressions when compared with the non-IPA tissues. Compared with the blank control and empty plasmid groups, the miR-145 mimic group showed significantly decreased PI3K, AKT3, mTOR, S6K and RPS6 mRNA and protein expressions as well as phosphorylation levels; besides, the IPA cell proliferation, migration and invasion ability were strongly inhibited, accompanied with the increased number of apoptotic cells. In the miR-145 inhibitor group, the PI3K, AKT3, mTOR, S6K and RPS6 mRNA and protein expressions as well as the phosphorylation levels were significantly increased; cell proliferation, migration and invasion ability were remarkably elevated, accompanied with reduced apoptotic cell number. CONCLUSION: The study demonstrates that miR-145 inhibits the mTOR signaling pathway to suppress the IPA cell proliferation and invasion and promotes its apoptosis by targeting AKT3.

Endovascular Perforation Murine Model of Subarachnoid Hemorrhage.

Subarachnoid hemorrhage (SAH) is a subtype of stroke with disastrous outcomes of high disability and mortality. A variety of endeavors have been developed to explore a SAH animal model for investigation of the disease. Among these models, the endovascular perforation SAH model was considered to be the most simulative to the clinical human SAH because it reproduces several pathophysiology procedures and presents some of the most important post-hemorrhage features. An applicable SAH animal model should have the characteristics of low mortality rate, limited surgical manipulation, and adaptation to many species, which permits reproducibility and standardization. An intensive discussion of how to improve the techniques and refine the procedure has taken place in the last decade. This report describes our experiences with a murine model of SAH. We aim to standardize and optimize the procedures to establish a relatively stable animal model for SAH research.

Microsurgery with or without Neuroendoscopy in Petroclival Meningiomas.

AIM: This study aimed to investigate the operative procedure for neuroendoscope-assisted microscopic resection of petroclival meningioma to improve prognosis. MATERIAL AND METHODS: Twelve patients with petroclival meningioma who had undergone neuroendoscope-assisted microscopic resection at the Department of Neurosurgery, First Affiliated Hospital of Xinjiang Medical University were selected. In addition, 12 patients with petroclival meningioma who had undergone microscopic surgery were used as control. Clinical data from the 24 cases of petroclival meningioma were analyzed. RESULTS: For the neuroendoscope-assisted group, six, five, and one cases were respectively subjected to total resection, subtotal resection, and most resection. For the microscopic surgery group, two, three, and seven cases were respectively subjected to total resection, subtotal resection, and most resection. Both the total and subtotal resection rates of petroclival meningioma in the neuroendoscope-assisted group were significantly higher than those in the microscopic surgery group (p < 0.05). No difference was observed for short-term and long-term complications (p > 0.05) between the two groups. CONCLUSION: Neuroendoscope-assisted microscopic resection for petroclival meningioma can improve the total and subtotal resection rates of the tumor. Moreover, this method does not increase postoperative short-term and long-term complications.