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ObjectiveTo investigate the effect of modified Xiaoyaosan on central dopamine transporter （DAT）/protein kinase C （PKC）-dependent signaling pathway in hyperprolactinemia （HPRL） rats. MethodHPRL rat model was established by chronic combined stress combined with intraperitoneal injection of metoclopramide. Ninety-six rats were randomly divided into six groups， namely， the blank group， model group， western medicine （bromocriptine， 0.001 g·kg-1·d-1） group， and high-， medium-， and low-dose （60， 30， 15 g·kg-1·d-1） modified Xiaoyaosan groups. After 14 days of administration， the serum prolactin （PRL） content was detected by enzyme-linked immunosorbent assay， the expression of tyrosine hydroxylase （TH） in rat hypothalamus by immunohistochemistry， and the protein expression of DAT and PKC in hypothalamus by Western blot. ResultCompared with the blank group， the model group exhibited significantly increased PRL and DAT （P<0.01）， but decreased TH and PKC （P<0.01）. Compared with the model group， bromocriptine and modified Xiaoyaosan at the medium dose significantly lowered the content of PRL （P<0.01）. The modified Xiaoyaosan at the medium and high doses elevated the expression of TH （P<0.05， P<0.01）. The expression levels of PKC in the medium- and low-dose modified Xiaoyaosan groups and the western medicine group were significantly increased （P<0.01）， while the DAT expression levels in the high-， medium-， and low-dose modified Xiaoyaosan groups and the western medicine group were decreased （P<0.01）. ConclusionThe modified Xiaoyaosan is able to up-regulate the expression of TH and down-regulate the level of DAT through PKC-dependent signaling pathway， thereby regulating the PRL.
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Long noncoding RNAs (lncRNAs) are noncoding RNAs more than 200 nucleotides in length. A growing number of reports indicate that lncRNAs play a key role in multiple cancers by serving as oncogenes or tumor suppressor genes. MAGI2 antisense RNA 3 (MAGI2-AS3) is ubiquitously expressed in human cancers, and the level of MAGI2-AS3 expression is associated with the progression and prognosis of cancers. Moreover, dysregulation of MAGI2-AS3 has been found to regulate cancer cell proliferation, cell death, invasion and metastasis and treatment resistance by serving as a competing endogenous RNA (ceRNA), epigenomic regulator, and transcriptional regulator. Moreover, increasing evidence shows that MAGI2-AS3 may be a potential biomarker for cancer prognosis and a potential target for cancer therapy. In this review, we summarize current research on the functions, mechanisms and clinical significance of the lncRNA MAGI2-AS3 in cancer development.
Assuntos
Neoplasias/genética , RNA Longo não Codificante/genética , Proteínas Adaptadoras de Transdução de Sinal/genética , Biomarcadores/análise , Progressão da Doença , Guanilato Quinases/genética , Humanos , PrognósticoRESUMO
Ski is an evolutionary conserved protein, which is involved in diverse cellular processes such as proliferation, differentiation, transformation and tumor progression. In spinal cord injury, the activation of astrocytes and reactive astrocyte hyperplasia are important factors affecting the formation of glial scar after spinal cord injury. Ski is highly expressed after spinal cord injury, and acts on astrocytes through transforming growth factor-beta, mitogen-activated protein kinase and other signaling pathways, and regulates their activation, proliferation, migration and glial scar formation, providing a new therapeutic direction for the treatment of spinal cord injury.
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The studies of Botulinum toxin A (BoNT/A) are progressing in many fields. BoNT/A has been used in neurological disorders, such as pains, spasticity, dystonias and autonomic disorders, etc. The pharmacological interaction among BoNT/A, neuronal transport and protein has been explored, and promoted basic science studies.
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After spinal cord injury, the formation of glial scar related to the hypertrophy, proliferation and migration of astrocytes, and the increased expression of glial fibers acidic protein, vimentin and nestin, etc., and it may also inhibit the growth of neuron axon.
