American journal of translational research
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Peripheral neuropathic pain is a complex disease, and treated based on underlying diseases. Emerging evidences suggest that hyperbaric oxygen alleviates neuropathic pain. However, its cellular and molecular mechanism on pain relief is unknown. ⋯ In contrast, chloroquine, an autophagy inhibitor, counteracted hyperbaric oxygen analgesic effect. These findings indicate that hyperbaric oxygen attenuated neuropathic pain by increasing spinal autophagic flux via inhibiting mTOR pathway. Our study provides pre-clinical evidences in expediting hyperbaric oxygen become a safe clinical treatment of neuropathic pain.
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Currently sevoflurane is the volatile anesthetic most wildly used in pediatric surgery. Whether neonatal exposure to sevoflurane brings about a long-lasting adverse impact even at juvenile and adult age, attracts extensive concerns. However, to date the consensus has not been reached and how exposure to sevoflurane in early life affects long-term ability of learning and memory is not fully elucidated. ⋯ Pair-pulse facilitation (PPF) ratio in group SEV at juvenile and adult age was augmented to varying extent. These effects were most noticeable at juvenile stage with tendency of alleviation during adulthood. The present study provides an alternative explanation for the mechanism underlying developmental neurotoxicity of sevoflurane, which may ameliorate future preventive and therapeutic strategies.
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We investigated the ability of microRNA-93 (miR-93) to influence proliferation, invasion, migration, and apoptosisofrenal cell carcinoma (RCC) cells via transforming growth factor-β/solvated metal atom dispersed (TGF-β/Smad) signaling by targeting runt-related transcription factor 3 (RUNX3). RCC tissues with corresponding adjacent normal tissues were collected from 249 RCC patients. And normal renal tissues were collected from patients without RCC who received nephrectomy. ⋯ Compared with inhibitor-NC group, proliferation, invasion, and migration reduced, while apoptosis increased, and cells at G0/G1 phase arrested in the miR-93 inhibitor group (all P<0.05). Compared with miR-93 inhibitor group, cell proliferation, invasion, and migration increased with increasing cells from G1 to S phase while the apoptosis decreased, in miR-93 inhibitor + si-RUNX3 group (all P<0.05). In conclusion, miR-93 inhibits apoptosis and promotes proliferation, invasion, and migration of RCC cells via TGF-β/Smad signaling by inhibiting RUNX3.
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Endoplasmic reticulum (ER) stress play important roles in the spinal cord injury (SCI), which including blood-spinal cord barrier (BSCB) disruption. Lithium chloride (LiCl) is a clinical drug for bipolar mood disorders and contributes to neuroprotection. This study aims to investigate the effects of LiCl on BSCB disruption and the ER stress pathway induced by spinal cord injury. ⋯ Our data indicated that LiCl treatment could attenuates BSCB disruption and improved the recovery of functional locomotion in rats SCI model, reduced the structure damage and number loss of microvessels, increased the expressions of junction proteins, including p120, β-catenin, occludin, and claudin-5, via reversed the upregulated ER stress associated proteins. In addition, LiCl significantly inhibited the increase of ER stress markers and prevents loss of junction proteins in thapsigargin (TG)-treated human brain microvascular endothelial cells (HBMEC). These findings suggest that LiCl treatment alleviates BSCB disruption and promote the neurological function recovery after SCI, partly through inhibiting the activation of ER stress.