White crystalline powder
Prod. by Streptomyces hygroscopicus NRRL 5491
Methanol; Chloroform; Ethyl Acetate
973.0±75.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
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Autophagy plays an important role in the pathogenesis of acute kidney injury (AKI). Although autophagy activation was shown to be associated with an increased lifespan and beneficial effects in various pathologies, the impact of autophagy activators, particularly, rapamycin and its analogues on AKI remains obscure. In our study, we explored the effects of rapamycin treatment in in vivo and in vitro models of ischemic and cisplatin-induced AKI. The impact of rapamycin on the kidney function after renal ischemia/reperfusion (I/R) or exposure to the nephrotoxic agent cisplatin was assessed by quantifying blood urea nitrogen and serum creatinine and evaluating the content of neutrophil gelatinase-associated lipocalin, a novel biomarker of AKI. In vitro experiments were performed on the primary culture of renal tubular cells (RTCs) that were subjected to oxygen-glucose deprivation (OGD) or incubated with cisplatin under various rapamycin treatment protocols. Cell viability and proliferation were estimated by the MTT assay and real-time cell analysis using an RTCA iCELLigence system. Although rapamycin inhibited mTOR (mammalian target of rapamycin) signaling, it failed to enhance the autophagy and to ameliorate the severity of AKI caused by ischemia or cisplatin-induced nephrotoxicity. Experiments with RTCs demonstrated that rapamycin exhibited the anti-proliferative effect in primary RTCs cultures but did not protect renal cells exposed to OGD or cisplatin. Our study revealed for the first time that the mTOR inhibitor rapamycin did not prevent AKI caused by renal I/R or cisplatin-induced nephrotoxicity and, therefore, cannot be considered as an ideal mimetic of the autophagy-associated nephroprotective mechanisms (e.g., those induced by caloric restriction), as it had been suggested earlier. The protective action of such approaches like caloric restriction might not be limited to mTOR inhibition and can proceed through more complex mechanisms involving alternative autophagy-related targets. Thus, the use of rapamycin and its analogues for the treatment of various AKI forms requires further studies in order to understand potential protective or adverse effects of these compounds in different contexts.
Rapamycin Is Not Protective against Ischemic and Cisplatin-Induced Kidney Injury.
Andrianova NV1,2, Zorova LD2,3, Babenko VA2,3, Pevzner IB2,3, Popkov VA2,3, Silachev DN2,3, Plotnikov EY4,3,5, Zorov DB6,3.
[mTOR inhibitors, autophagia and Cancer: looking forward to a universal financial coverage].
Arancibia J1, Labbe TP1, Rios JA1.
To investigate the role of mammalian target of rapamycin (mTOR) activation in menthol-induced expression of airway inflammation- related factors in human bronchial epithelial cells and explore its mechanism.
Cultured human bronchial epithelial cells (BEAS-2B) were divided into normal control group, menthol group, rapamycin group, and menthol+rapamycin group with corresponding treatments. The cell viability was measured with CCK-8 method. The mRNA levels of transient receptor potential melastatin 8 (TRPM8), tumor necrosis factor (TNF)-α and interleukin (IL)-1β were detected by RT-PCR, and the protein expressions of phosphorylated mTOR (p-mTOR), TRPM8, TNF-α and IL-1β were determined using Western blotting. The intracellular Ca2+ fluorescence intensity was measured by flow cytometry.
Compared with the normal control cells, menthol- treated cells showed significantly increased TNF-α, IL-1β, and p-mTOR expression and elevated intracellular Ca2+ concentration (P < 0.05), and the rapamycin-treated cells exhibited significantly decreased p-mTOR expression (P < 0.05). No significant difference was found in TNF-α, IL-1β or intracellular Ca2+ concentration between the normal control and rapamycin-treated cells (P>0.05). Compared with the menthol-treated cells, the cells treated with both menthol and rapamycin showed significantly decreased TNF- α, IL-1β, and p-mTOR expression and obviously lowered intracellular Ca2+ concentration (P < 0.05).
Menthol promotes the expressions of airway inflammationrelated factors IL-1β and TNF-α possibly by activating mTOR to cause the increase of intracellular Ca2+ concentration.
airway inflammation; human bronchial epithelial cells; mammalian target of rapamycin; menthol; transient receptor potential melastatin 8
[Role of mammalian target of rapamycin activation in menthol-induced expressions of airway inflammation-related factors in human bronchial epithelial cells in vitro].
Chen H1, Li M1.
2019 Nov 30
Rapamycin (Sirolimus) is a potent and specific mTOR inhibitor with an IC50 of 0.1 nM.