Lipoprotein lipase: Biosynthesis, regulatory factors, and its role in atherosclerosis and other diseases.

Lipoprotein lipase (LPL) is a rate-limiting enzyme that catalyzes hydrolysis of the triglyceride (TG) core of circulating TG-rich lipoproteins including chylomicrons (CM), low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL). A variety of parenchymal cells can synthesize and secrete LPL. Recent studies have demonstrated that complicated processes are involved in LPL biosynthesis, secretion and transport.

Exacerbation of diabetic cardiac hypertrophy in OVE26 mice by angiotensin II is associated with JNK/c-Jun/miR-221-mediated autophagy inhibition.

Both diabetes and angiotensin II (Ang II) excess trigger cardiac remodeling and dysfunction, and diabetic cardiomyopathy. We hypothesized that cardiac hypertrophy associated with the development of diabetic cardiomyopathy is worsened by increased Ang II. Male type 1 diabetic OVE26 and wild-type mice were given Ang II (sc.

Synthesis, characterization, and sustained release property of FeO@(enrofloxacin-layered double hydroxides) nanocomposite.

A novel magnetic nanocomposite with enrofloxacin (ENR) intercalated MgAl layered double hydroxides (LDH) coated on FeO particles, denoted as FeO@(ENR-LDH), was assembled via a delamination-reassembling process. FeO@(ENR-LDH) was characterized by powder X-ray diffraction, Fourier transform infrared spectroscopy, element chemical analysis, transmission electron microscopy, differential scanning calorimetry, and room-temperature magnetic measurements. Results showed the following: ① FeO@(ENR-LDH) consisted of both ENR-LDH nanocrystallite and FeO phases; ② FeO@(ENR-LDH) presented well-defined core-shell structure with diameter in the range of 15-20nm; ③ the thermal stability of ENR was enhanced after intercalation; and ④ FeO@(ENR-LDH) exhibited good superparamagnetism.

Action of a Novel PDE4 inhibitor ZL-n-91 on lipopolysaccharide-induced acute lung injury.

In the present study, we investigated the effect of classic PDE4 inhibitor rolipram and novel PDE4 inhibitor ZL-n-91 on LPS-induced acute lung injury (ALI) in mice and its mechanism. ALI was induced in ICR mice by instilling intratracheally with LPS, and mice were divided into seven groups: control (Saline), LPS group, ZL-n-91 (3 microg, 10 microg, and 30 microg kg(-1), ip), Rolipram (1.0 mg kg(-1), ip) and dexamethasone (0.