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Paradoxical Sleep (ps) Factors
Published in Shojiro Inoué, Biology of Sleep Substances, 2020
Drucker-Colín et al.24 also reported the enhancement of PS during the first 3-h period following rat GH administration (0.1 to 1 mg/kg i.p.) in rats. It was further noted that PS reduction induced by anisomycin, a protein synthesis inhibitor, was blocked by the concurrent administration of GH.
Proto-Oncogene and Onco-Suppressor Gene Expression
Published in Enrique Pimentel, Handbook of Growth Factors, 2017
The use of specific inhibitors may contribute to elucidation of the mechanisms of regulation of gene expression by growth factors and other extracellular stimuli. The application of the protein synthesis inhibitor cycloheximide in serum-stimulated human and murine cells suggests that an unstable protein is involved in modulating the expression of cell cycle-associated genes,540 including the expression of c-fos and c-myc.535 The effects of the protein kinase inhibitor, 2-aminopurine, suggest that a protein kinase may be involved in serum-stimulated c-fos and c-myc expression as well as in the induction of the IFN-β gene by viruses or synthetic double-stranded RNAs.541 The use of the protein synthesis inhibitor anisomycin indicates that the regulatory mechanisms of c-fos and c-myc gene expression induced by growth factors may be different in different types of cells.163 Thus, there are multiple levels and mechanisms through which c-fos and c-myc gene expression is regulated.
Host-directed antileishmanial interventions: Harvesting unripe fruits to reach fruition
Published in International Reviews of Immunology, 2023
Members of the MAPK pathway that activate transcription factors for several pro-inflammatory cytokines are also exploited by the parasite [44]. In one study, immunomodulatory agent, fucoidan was found to restore functional MAPK/NF-κB pathway in L. donovani-infected macrophages, leading to NO production and polarized Th1 responses [45]. Furthermore, treatment with p38 activator, anisomycin brought about rapid clearance in infected macrophages by restoring the NO-generating effects of p38 phosphorylation in infected host [46]. The NO-generating effect of nonsteroidal anti-inflammatory drugs (NSAIDs) too has been employed in the control of murine visceral leishmaniasis. For instance, orally administered acetyl salicylic acid (ASA) following lesion development inhibited L. major parasite visceralization and reduced lesion size, further highlighting nitric oxide as a critical element of host protection during infection [47].
The Role of C-Jun N-terminal Kinase-1 in Controlling Aquaporin-1 and Choroidal Thickness during Recovery from Form-deprivation Myopia in Guinea Pigs
Published in Current Eye Research, 2021
Wei Chen, Zhiwei Li, Qimiao Wang, Yan Wang, Yue Zhang
The animals wore the face mask for 21 days to induce myopia. Then, the face masks were removed, and the guinea pigs were re-exposed to the normal visual environment. Ninety-six guinea pigs were divided into four groups: the recovery group (REC, n = 24), the REC plus SP600125 group (REC-SP, n = 24), the REC plus anisomycin group (REC-AN, n = 24) and the REC plus dimethyl sulfoxide (DMSO) group (vehicle) (REC-DM, n = 24). SP600125 (Abcam, Cambridge, MA, USA) and anisomycin (Abcam, Cambridge, MA, USA) were injected into the REC-SP group and the REC-AN group, respectively, with the same concentration and volume (0.2 nmol, 0.01 ml). SP600125, which is an inhibitor of JNK, and anisomycin, which is an agonist of JNK, were both dissolved in DMSO and diluted with PBS to their final concentrations. In the REC-DM group, the form-deprived eyes were injected with sterilized DMSO solution (0.01 ml, diluted with PBS), which is the carrier. All intravitreal injections were performed once using a microinjector (Shanghai Meter Glass Factory, Shanghai, China) with a 30-gauge needle at 1.5 mm posterior to the temporal limbus under anesthesia with 95 mg/kg pentobarbital (intraperitoneal injection) when the face masks were removed. In the REC group, the guinea pigs were raised without any injection after the face mask was removed. Moreover, the normal control group (NC) included 32 guinea pigs that were free of form deprivation and were left untreated.
Tanshinone IIA inhibits osteosarcoma growth through modulation of AMPK-Nrf2 signaling pathway
Published in Journal of Receptors and Signal Transduction, 2020
Zengjun Xie, Binbin He, Ziyun Jiang, Liang Zhao
There are many drugs have been investigated to regulate the viability of osteosarcoma. For example, marrubenol inhibits osteosarcoma cancer growth through inducing autophagic cell death [38,39]. Anisomycin is able to induce cycle arrest and apoptosis through regulation of mitochondrial biogenesis in osteosarcoma [40]. Icarisid II has been found to regulate cancer proliferation in human osteosarcoma [41]. In addition, osteosarcoma cell energy metabolism and invasion capacity are also under the control of gambogic acid [42]. Similar to these results, this study explored the influence of Tan IIA on osteosarcoma viability, migration, and proliferation. Our study not only observed the proapoptotic effect of Tan IIA on osteosarcoma but also confirmed the anti-invasion effect of Tan IIA. These results indicate that cancer biological features of osteosarcoma could be comprehensive regulated by Tan IIA. In fact, several previous studies have reported the antitumor actions of Tan IIA. For example, cervical cancer glucose metabolism is controlled by Tan IIA [43]. Gastric cancer proliferation and tumor growth are inhibited by Tan IIA [44]. The chemosensitivity of nonsmall-cell lung cancer could be enhanced by Tan IIA [45]. The oncogene expression of liver cancer is affected by Tan IIA [4]. Colorectal cancer viability and mitochondrial performance are modulated by Tan IIA [46]. Similar to the previous studies, our results add more information about the anticancer impacts of Tan IIA. However, more animal studies or clinical trials are required to support our finding.