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Background: The current research on advanced glycosylation end products (AGEs) and cognitive function is limited. Objective: We aimed to investigate the relationship between multiple plasma AGEs and cognitive function and mild cognitive impairment (MCI). Methods: Baseline data from The Lifestyle and Healthy Aging of Chinese Square Dancer Study was used in this cross-sectional study. Ultra-high-performance liquid chromatography tandem mass spectrometry was used to determine plasma levels of carboxymethyl lysine (CML), carboxyethyl lysine (CEL), and methyl imidazolinone (MG-H1). Four cognitive tests were used to obtain the four cognitive domain scores and the composite z scores. The Petersen criteria were used to diagnose MCI. The data were analyzed by multivariable linear and logistic regression models. Results: This study included 1,018 participants (median age 61.0 years, 87.3% female). After multivariate adjustment, the βs of the highest quartile of CML and CEL compared to the lowest quartile were –0.28 (–0.38, –0.17) and –0.13 (–0.23, –0.03), respectively, for the composite z score. For the four cognitive domains, CML was negatively correlated with memory, attention, and executive function, and CEL was negatively associated with memory and language function. In addition, higher CML was associated with a higher odds of MCI. MG-H1 was not associated with cognitive function. Conclusions: High plasma AGE levels were correlated with poorer cognitive function, particularly CML and CEL, higher levels of CML were also associated with higher odds of MCI. To clarify the effects of different AGEs on cognitive function and the underlying mechanisms, further longitudinal and experimental studies are needed. [ABSTRACT FROM AUTHOR]

A range of indolizines and H‐phosphonates smoothly underwent Mn(OAc)3‐mediated C‐H phosphonylation procedure to afford the phosphorylated indolizines in good to excellent yields with high regioselectivities. Mechanistic studies have been conducted to clarify the radical pathway. A series of phosphorylated indolizines were facilely synthesized via Mn(OAc)3‐mediated C−H phosphonylation of indolizines with H‐Phosphonates at simple conditions. [ABSTRACT FROM AUTHOR]

Pathological cardiac hypertrophy is a maladaptive response in a variety of organic heart disease (OHD), which is characterized by mitochondrial dysfunction that results from disturbed energy metabolism. SIRT3, a mitochondria-localized sirtuin, regulates global mitochondrial lysine acetylation and preserves mitochondrial function. However, the mechanisms by which SIRT3 regulates cardiac hypertrophy remains to be further elucidated. In this study, we firstly demonstrated that expression of SIRT3 was decreased in Angiotension II (Ang II)-treated cardiomyocytes and in hearts of Ang II-induced cardiac hypertrophic mice. In addition, SIRT3 overexpression protected myocytes from hypertrophy, whereas SIRT3 silencing exacerbated Ang II-induced cardiomyocyte hypertrophy. In particular, SIRT3-KO mice exhibited significant cardiac hypertrophy. Mechanistically, we identified NMNAT3 (nicotinamide mononucleotide adenylyltransferase 3), the rate-limiting enzyme for mitochondrial NAD biosynthesis, as a new target and binding partner of SIRT3. Specifically, SIRT3 physically interacts with and deacetylates NMNAT3, thereby enhancing the enzyme activity of NMNAT3 and contributing to SIRT3-mediated anti-hypertrophic effects. Moreover, NMNAT3 regulates the activity of SIRT3 via synthesis of mitochondria NAD. Taken together, these findings provide mechanistic insights into the negative regulatory role of SIRT3 in cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

The pinning synchronization problem for a class of complex networks is studied by a stochastic viewpoint, in which both time-varying coupling strength and nondelayed and delayed coupling are included. Different from the traditionally similar methods, its interval is separated into two subintervals and described by a Bernoulli variable. Both bounds and switching probability of such subintervals are contained. Particularly, the nondelayed and delayed couplings occur alternately in which another independent Bernoulli variable is introduced. Then, a new kind of pinning controller without time-varying coupling strength signal is developed, in which only its bounds and probabilities are contained. When such probabilities are unavailable, two different kinds of adaption laws are established to make the complex network globally synchronous. Finally, the validity of the presented methods is proved through a numerical example. [ABSTRACT FROM AUTHOR]

Liver cells are easily damaged by oxidative stress during progression both in liver development and throughout adult life, resulting in tissue pathology that ranges from simple hepatitis to nonalcoholic fatty liver disease. In this study, we determined the attenuation of oxidative stress in liver cells with pretreatment of rosmarinic acid (RA), which is an antioxidant agent from Rosmarinus officinalis. The human liver cell line L02 was damaged by hydrogen peroxide (H2O2). In the RA treatment group, the viability of L02 cells increased and the intracellular reactive oxygen species levels decreased compared with the H2O2-induced damage group. Analysis of flow cytometry revealed that the percentage of G2/M cell cycle arrest and cell apoptosis decreased in the RA treatment group. This alteration was associated with activation of a G2/M DNA damage and oxidative stress apoptotic signal. Furthermore, we determined the redox-sensitive protein expression of mitogen-activated protein kinases (MAPKs), quinone acceptor oxidoreductase 1 (NQO1), and nuclear factor E2-related factor 2 (Nrf2), and the expression of both MAPKs and Nrf2 was activated in the RA group. Results showed that the relevant protein expression of MAPKs and Nrf2 was activated in the RA group. Thus, RA protected L02 cells from oxidative damage through suppressing cell cycle arrest and cell apoptosis with the activation of MAPK and Nrf2 signaling pathways. [ABSTRACT FROM AUTHOR]

Silent mating type information regulation 2 homolog 3 (SIRT3) is a major protective mediator that ameliorates oxidative stress and mitochondrial dysfunction, which are associated with the pathogenesis of epithelial-mesenchymal transition (EMT). The present study was aimed to investigate the potential role of SIRT3 in renal tubular EMT both in vitro and in vivo . Firstly, we showed that the expression of SIRT3 was repressed in angiotensin II-induced EMT. SIRT3 deficiency triggered EMT response, while over-expression of SIRT3 attenuated EMT response. In addition, over-expression of SIRT3 repressed AngⅡ-induced excessive production of mitochondrial superoxide, as well as mitochondrial dysfunction evidenced by the maintenance of mitochondrial number and morphology, and the stabilization of mitochondrial membrane potential. In conclusion, these findings identify a protective role of SIRT3 against angiotensin II-induced EMT in the kidney, and suggest SIRT3 upregulation is a potential therapeutic strategy for the treatment of renal tubulointerstitial fibrosis. [ABSTRACT FROM AUTHOR]

Highlights: [•] Elevated NF-κB activity in neonatal rat cardiomyocytes overexpressing RIP140. [•] RIP140 impacts proinflammatory response of cardiomyocytes via p65-NF-κB pathway. [•] p65-NF-κB is involved in RIP140-induced metabolic dysregulation in cardiomyocytes. [ABSTRACT FROM AUTHOR]

Receptor-interacting protein 140 (RIP140) is a multifunctional coregulator of lipid metabolism and inflammation. However, the potential role of RIP140 in atherosclerosis remains unknown. The present study investigated the impact of RIP140 on foam cell formation, a critical step in pathogenesis of atherosclerosis. The expression of RIP140 was increased in foam cells. RIP140 overexpression resulted in decreased cholesterol efflux in macrophages and their concomitant differentiation into foam cells. Moreover, RIP140 negatively regulated the macrophage expression of ATP-binding cassette transporters A1 and G1 (ABCA1/G1), by suppressing the expression and activity of liver X receptor (LXR). These findings shed light onto the contribution of RIP140 to the development and progression of atherosclerosis, and suggest a novel therapeutic target for the treatment of atherosclerosis. [ABSTRACT FROM AUTHOR]

Highlights: [•] Salvianolic acid B (SalB) protected cardiomyocytes from AngII-induced hypertrophy. [•] SalB’ anti-hypertrophy was partly attributed to its inhibition on PARP-1. [•] SalB prevented the depletion of cellular NAD+ induced by AngII. [•] SalB’s antioxidant effect might contribute to the inhibition of PARP-1. [ABSTRACT FROM AUTHOR]