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181.
The purpose of this research was to study whether the bioavailability of lovastatin could be improved by administering lovastatin
solid lipid nanoparticles (SLN) duodenally to rats. Lovastatin SLN were developed using triglycerides by hot homogenization
followed by ultrasonication. Particle size and zeta potential were measured by photon correlation spectroscopy. The solid
state of the drug in the SLN and lipid modification were characterized. Bioavailability studies were conducted in male Wistar
rats after intraduodenal administration of lovastatin suspension and SLN. Stable lovastatin SLN having a mean size range of
60 to 119 nm and a zeta potential range of −16 to −21 mV were developed. More than 99% of the lovastatin was entrapped in
the SLN. Lovastatin was dispersed in an amorphous state, and triglycerides were in {ieE162-1} form in the SLN. In vitro stability
studies showed the slow release and stability of lovastatin SLN. The relative bioavailabilities of lovastatin and lovastatin
hydroxy acid of SLN were increased by ∼173% and 324%, respectively, compared with the reference lovastatin suspension.
Published: March 23, 2007 相似文献
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Paul Prajita Patel Paritosh Verma Suresh K. Mishra Pragyan Sahu Bikash R. Panda Pritam Kumar Kushwaha Gajraj Singh Senapati Shantibhusan Misra Namrata Suar Mrutyunjay 《Cell biology and toxicology》2022,38(1):111-127
Cell Biology and Toxicology - The key to bacterial virulence relies on an exquisite balance of signals between microbe and hosts. Bacterial toxin–antitoxin (TA) system is known to play a... 相似文献
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Selenocysteine (Sec) is inserted into proteins by recoding a UGA stop codon followed by a selenocysteine insertion sequence (SECIS). UGA recoding by the Sec machinery is believed to be very inefficient owing to RF2-mediated termination at UGA. Here we show that recoding efficiency in vivo is 30–40% independently of the cell growth rate. Efficient recoding requires sufficient selenium concentrations in the medium. RF2 is an unexpectedly poor competitor of Sec. We recapitulate the major characteristics of SECIS-dependent UGA recoding in vitro using a fragment of fdhF-mRNA encoding a natural bacterial selenoprotein. Only 40% of actively translating ribosomes that reach the UGA codon insert Sec, even in the absence of RF2, suggesting that the capacity to insert Sec into proteins is inherently limited. RF2 does not compete with the Sec incorporation machinery; rather, it terminates translation on those ribosomes that failed to incorporate Sec. The data suggest a model in which early recruitment of Sec-tRNASec–SelB–GTP to the SECIS blocks the access of RF2 to the stop codon, thereby prioritizing recoding over termination at Sec-dedicated stop codons. 相似文献
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Qing-Yin Wang Hongping Dong Bin Zou Ratna Karuna Kah Fei Wan Jing Zou Agatha Susila Andy Yip Chao Shan Kim Long Yeo Haoying Xu Mei Ding Wai Ling Chan Feng Gu Peck Gee Seah Wei Liu Suresh B. Lakshminarayana CongBao Kang Julien Lescar Francesca Blasco Paul W. Smith Pei-Yong Shi 《Journal of virology》2015,89(16):8233-8244
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Li Jing Mao-Tao He Yue Chang Suresh L. Mehta Qing-Ping He Jian-Zhong Zhang P. Andy Li 《International journal of biological sciences》2015,11(1):59-66
Coenzyme Q10 (CoQ10) acts by scavenging reactive oxygen species to protect neuronal cells against oxidative stress in neurodegenerative diseases. The present study was designed to examine whether CoQ10 was capable of protecting astrocytes from reactive oxygen species (ROS) mediated damage. For this purpose, ultraviolet B (UVB) irradiation was used as a tool to induce ROS stress to cultured astrocytes. The cells were treated with 10 and 25 μg/ml of CoQ10 for 3 or 24 h prior to the cells being exposed to UVB irradiation and maintained for 24 h post UVB exposure. Cell viability was assessed by MTT conversion assay. Mitochondrial respiration was assessed by respirometer. While superoxide production and mitochondrial membrane potential were measured using fluorescent probes, levels of cytochrome C (cyto-c), cleaved caspase-9, and caspase-8 were detected using Western blotting and/or immunocytochemistry. The results showed that UVB irradiation decreased cell viability and this damaging effect was associated with superoxide accumulation, mitochondrial membrane potential hyperpolarization, mitochondrial respiration suppression, cyto-c release, and the activation of both caspase-9 and -8. Treatment with CoQ10 at two different concentrations started 24 h before UVB exposure significantly increased the cell viability. The protective effect of CoQ10 was associated with reduction in superoxide, normalization of mitochondrial membrane potential, improvement of mitochondrial respiration, inhibition of cyto-c release, suppression of caspase-9. Furthermore, CoQ10 enhanced mitochondrial biogenesis. It is concluded that CoQ10 may protect astrocytes through suppression of oxidative stress, prevention of mitochondrial dysfunction, blockade of mitochondria-mediated cell death pathway, and enhancement of mitochondrial biogenesis. 相似文献