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Oral cavity: An open horizon for nanopharmaceuticals
Nguyen Oanh Oanh Thi,Tran Khue Dan,Ha Nhan Thi,Doan Sang Minh,Dinh Thi Thanh Hai,Tran Tuan Hiep 한국약제학회 2021 Journal of Pharmaceutical Investigation Vol.51 No.4
Background Oral administration is the primary route employed for drug delivery. In addition to the gastrointestinal tract, the oral cavity has been drawing considerable attention owing to its physiological properties and advances in drug carrier development. Notably, nanotechnology has made immense contributions to enhancing drug bioavailability, stability, and efficacy, both in research and clinical settings. Area covered The present review comprises lessons from physiological characteristics to fundamental material science knowledge, summarizing the pros and cons of nanotechnology applications in therapeutic drug delivery. The oral cavity presents inherent challenges, including oral cancer, dental caries, oral infection, or oral inflammation, that necessitate local solutions. Simultaneously, the vascular system under the tongue and in the buccal region offers a portal for systemic drug absorption. Expert opinion Among available delivery systems, nanoparticle-based drug delivery, with the oral cavity as the action or absorption site, can be developed as a principal dosage formulation. Although convenience and fast onset might be advantageous, additional studies are warranted for preclinical characterization, especially in animal models, and for determining manufacturing competence, prior to human trials to meet standards in clinical settings.
Mitochondria elongation is mediated through SIRT1-mediated MFN1 stabilization
Oanh, N.T.K.,Park, Y.Y.,Cho, H. Pergamon Press ; Elsevier Science Ltd 2017 Cellular signalling Vol.38 No.-
Mitochondria are highly dynamic organelles that change size and morphology by fusing together or dividing through fission. In response to cellular cues, signaling cascades may post-translationally modify mitochondria-shaping proteins, which lead to a change in mitochondria morphology. Here we show that nicotinamide (NAM), an inhibitor of sirtuin deacetylases, promotes degradation of mitochondria fusion protein mitofusin 1 (MFN1), suggesting that acetylation status of MFN1 is important for its protein stability. TIP60 but not PCAF acetyltransferase caused a reduction of MFN1 level. Meanwhile, siRNA-mediated knockdown of SIRT1 deacetylase caused a significant reduction of MFN1 whereas over-expression of SIRT1 increased its level in 293T cells. In vitro acetylation experiments showed that TIP60 increased the acetylation of MFN1 that was abolished by co-existence of SIRT1. Notably, MFN1 and SIRT1 levels were accumulated, along with mitochondria elongation under hypoxic conditions. Thus, the data suggest that mitochondria elongation under hypoxic condition is regulated through SIRT1-mediated MFN1 deacetylation and accumulation. The data provide an insight in the maintenance of cellular homeostasis through mitochondria morphological change.