Ginsenoside Rg1 alleviates A deposition by inhibiting NADPH oxidase 2 activation in APP/PS1 mice

Han Zhang,Yong Su,Zhenghao Sun,Ming Chen,Yuli Han,Yan Li,Xianan Dong,Shixin Ding,Zhirui Fang,Weiping Li,Weizu Li 고려인삼학회 2021 Journal of Ginseng Research Vol.45 No.6

Background: Ginsenoside Rg1 (Rg1), an active ingredient in ginseng, may be a potential agent for thetreatment of Alzheimer’s disease (AD). However, the protective effect of Rg1 on neurodegeneration in ADand its mechanism of action are still incompletely understood. Methods: Wild type (WT) and APP/PS1 AD mice, from 6 to 9 months old, were used in the experiment. The open field test (OFT) and Morris water maze (MWM) were used to detect behavioral changes. Neuronal damage was assessed by hematoxylin and eosin (H&E) and Nissl staining. Immunofluorescence,western blotting, and quantitative real-time polymerase chain reaction (q-PCR) were used toexamine postsynaptic density 95 (PSD95) expression, amyloid beta (Ab) deposition, Tau and phosphorylatedTau (p-Tau) expression, reactive oxygen species (ROS) production, and NAPDH oxidase 2(NOX2) expression. Results: Rg1 treatment for 12 weeks significantly ameliorated cognitive impairments and neuronaldamage and decreased the p-Tau level, amyloid precursor protein (APP) expression, and Ab generation inAPP/PS1 mice. Meanwhile, Rg1 treatment significantly decreased the ROS level and NOX2 expression inthe hippocampus and cortex of APP/PS1 mice. Conclusions: Rg1 alleviates cognitive impairments, neuronal damage, and reduce Ab deposition byinhibiting NOX2 activation in APP/PS1 mice.

A Hybrid Recommendation System based on Fuzzy C-Means Clustering and Supervised Learning

( Li Duan ),( Weiping Wang ),( Baijing Han ) 한국인터넷정보학회 2021 KSII Transactions on Internet and Information Syst Vol.15 No.7

A recommendation system is an information filter tool, which uses the ratings and reviews of users to generate a personalized recommendation service for users. However, the cold-start problem of users and items is still a major research hotspot on service recommendations. To address this challenge, this paper proposes a high-efficient hybrid recommendation system based on Fuzzy C-Means (FCM) clustering and supervised learning models. The proposed recommendation method includes two aspects: on the one hand, FCM clustering technique has been applied to the item-based collaborative filtering framework to solve the cold start problem; on the other hand, the content information is integrated into the collaborative filtering. The algorithm constructs the user and item membership degree feature vector, and adopts the data representation form of the scoring matrix to the supervised learning algorithm, as well as by combining the subjective membership degree feature vector and the objective membership degree feature vector in a linear combination, the prediction accuracy is significantly improved on the public datasets with different sparsity. The efficiency of the proposed system is illustrated by conducting several experiments on MovieLens dataset.

Proline Metabolism in Neurological and Psychiatric Disorders

Yuxiao Yao,Weiping Han 한국분자세포생물학회 2022 Molecules and cells Vol.45 No.11

Proline plays a multifaceted role in protein synthesis, redox balance, cell fate regulation, brain development, and other cellular and physiological processes. Here, we focus our review on proline metabolism in neurons, highlighting the role of dysregulated proline metabolism in neuronal dysfunction and consequently neurological and psychiatric disorders. We will discuss the association between genetic and protein function of enzymes in the proline pathway and the development of neurological and psychiatric disorders. We will conclude with a potential mechanism of proline metabolism in neuronal function and mental health.

Pancreatic regulation of glucose homeostasis

Pia V Röder,Bingbing Wu,Yixian Liu,Weiping Han 생화학분자생물학회 2016 Experimental and molecular medicine Vol.48 No.-

In order to ensure normal body function, the human body is dependent on a tight control of its blood glucose levels. This is accomplished by a highly sophisticated network of various hormones and neuropeptides released mainly from the brain, pancreas, liver, intestine as well as adipose and muscle tissue. Within this network, the pancreas represents a key player by secreting the blood sugar-lowering hormone insulin and its opponent glucagon. However, disturbances in the interplay of the hormones and peptides involved may lead to metabolic disorders such as type 2 diabetes mellitus (T2DM) whose prevalence, comorbidities and medical costs take on a dramatic scale. Therefore, it is of utmost importance to uncover and understand the mechanisms underlying the various interactions to improve existing anti-diabetic therapies and drugs on the one hand and to develop new therapeutic approaches on the other. This review summarizes the interplay of the pancreas with various other organs and tissues that maintain glucose homeostasis. Furthermore, anti-diabetic drugs and their impact on signaling pathways underlying the network will be discussed.

High-Yield Synthesis of Single-Crystalline Gold Nano-octahedra

Li, Cuncheng,Shuford, Kevin ,L.,Park, Q.-Han,Cai, Weiping,Li, Yue,Lee, Eun ,Je,Cho, Sung ,Oh WILEY-VCH Verlag 2007 Angewandte Chemie Vol.46 No.18

<B>Graphic Abstract</B> <P>Pieces of eight: Single-crystalline Au nano-octahedra with well-defined shape and tunable size can be synthesized by a modified polyol process. The octahedral Au nanocrystals have sharp corners and display optical properties that are sensitive to the crystal sizes and the truncation of the tips. <img src='wiley_img/14337851-2007-46-18-ANIE200604167-content.gif' alt='wiley_img/14337851-2007-46-18-ANIE200604167-content'> </P>

Inhibition of miRNA-222-3p Relieves Staphylococcal Enterotoxin B-Induced Liver Inflammatory Injury by Upregulating Suppressors of Cytokine Signaling 1

Peng Zhang,Jingda Yu,Yifang Gui,Cui Sun,Weiping Han 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.11

Purpose: Staphylococcal enterotoxin B (SEB) has been well-documented to induce liver injury. miRNA-222-3p (miR-222-3p) wasimplicated in SEB-induced lung injury and several liver injuries. This study aimed to explore the role of miR-222-3p in SEB-inducedliver injury. Materials and Methods: Expression of miR-222-3p and suppressors of cytokine signaling 1 (SOCS1) was detected using real-timequantitative PCR and western blot. Liver injury was determined by levels of aspartate aminotransferase (AST), alanine aminotransferase(ALT), and inflammatory cytokines, numbers of infiltrating mononuclear cells using AST/ALT assay kit, enzyme-linked immunosorbentassay (ELISA), and hematoxylin-eosin staining, respectively. Target binding between miR-222-3p and SOCS1 waspredicted on targetScan software, and confirmed by luciferase reporter assay. Results: SEB induced liver injury in D-galactosamine (D-gal)-sensitized mice, as demonstrated by increased serum levels of ASTand ALT, elevated release of interferon-gamma (INF-γ), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IL-2, andpromoted infiltrating immune cells into liver. Expression of miR-222-3p was dramatically upregulated, and SOCS1 was downregulatedin SEB-induced liver injury both in mice and splenocytes. Moreover, miR-222-3p knockout (KO) mice exhibited alleviatedliver injury accompanied with SOCS1 upregulation. Besides, splenocytes under SEB challenge released less INF-γ, TNF-α, IL-6,and IL-2 during miR-222-3p knockdown. Mechanically, SOCS1 was targeted and downregulated by miR-222-3p. Upregulation ofSOCS1 attenuated INF-γ, TNF-α, IL-6, and IL-2 release in SEB-induced splenocytes; downregulation of SOCS1 could block thesuppressive role of miR-222-3p knockdown in SEB-induced splenocytes. Conclusion: Inhibition of miR-222-3p relieves SEB-induced liver inflammatory injury by upregulating SOCS1, thereby providingthe first evidence of miR-222-3p in SEB-induced liver injury.

HOXC10 suppresses browning of white adipose tissues

Yvonne Ng,Shi-Xiong Tan,Sook Yoong Chia,Hwee Yim Angeline Tan,Sin Yee Gun,Lei Sun,Wanjin Hong,Weiping Han 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-

Given that increased thermogenesis in white adipose tissue, also known as browning, promotes energy expenditure, significant efforts have been invested to determine the molecular factors involved in this process. Here we show that HOXC10, a homeobox domain-containing transcription factor expressed in subcutaneous white adipose tissue, is a suppressor of genes involved in browning white adipose tissue. Ectopic expression of HOXC10 in adipocytes suppresses brown fat genes, whereas the depletion of HOXC10 in adipocytes and myoblasts increases the expression of brown fat genes. The protein level of HOXC10 inversely correlates with brown fat genes in subcutaneous white adipose tissue of cold-exposed mice. Expression of HOXC10 in mice suppresses cold-induced browning in subcutaneous white adipose tissue and abolishes the beneficial effect of cold exposure on glucose clearance. HOXC10 exerts its effect, at least in part, by suppressing PRDM16 expression. The results support that HOXC10 is a key negative regulator of the process of browning in white adipose tissue.

Lipid-Overloaded Enlarged Adipocytes Provoke Insulin Resistance Independent of Inflammation

Kim, Jong In,Huh, Jin Young,Sohn, Jee Hyung,Choe, Sung Sik,Lee, Yun Sok,Lim, Chun Yan,Jo, Ala,Park, Seung Bum,Han, Weiping,Kim, Jae Bum American Society for Microbiology 2015 Molecular and cellular biology Vol.35 No.10

<P>In obesity, adipocyte hypertrophy and proinflammatory responses are closely associated with the development of insulin resistance in adipose tissue. However, it is largely unknown whether adipocyte hypertrophy <I>per se</I> might be sufficient to provoke insulin resistance in obese adipose tissue. Here, we demonstrate that lipid-overloaded hypertrophic adipocytes are insulin resistant independent of adipocyte inflammation. Treatment with saturated or monounsaturated fatty acids resulted in adipocyte hypertrophy, but proinflammatory responses were observed only in adipocytes treated with saturated fatty acids. Regardless of adipocyte inflammation, hypertrophic adipocytes with large and unilocular lipid droplets exhibited impaired insulin-dependent glucose uptake, associated with defects in GLUT4 trafficking to the plasma membrane. Moreover, Toll-like receptor 4 mutant mice (C3H/HeJ) with high-fat-diet-induced obesity were not protected against insulin resistance, although they were resistant to adipose tissue inflammation. Together, our <I>in vitro</I> and <I>in vivo</I> data suggest that adipocyte hypertrophy alone may be crucial in causing insulin resistance in obesity.</P>

Arp2/3 complex regulates adipogenesis by controlling cortical actin remodelling.

Yang, Wulin,Thein, Shermaine,Lim, Chun-Yan,Ericksen, Russell E,Sugii, Shigeki,Xu, Feng,Robinson, Robert C,Kim, Jae Bum,Han, Weiping Portland Press Ltd. 2014 Biochemical journal Vol.464 No.2

<P>Extensive actin cytoskeleton remodelling occurs during adipocyte development. We have previously shown that disruption of stress fibres by the actin-severing protein cofilin is a requisite step in adipogenesis. However, it remains unclear whether actin nucleation and assembly into the cortical structure are essential for adipocyte development. In the present study we investigated the role of cortical actin assembly and of actin nucleation by the actin-related protein 2/3 (Arp2/3) complex in adipogenesis. Cortical actin structure formation started with accumulation of filamentous actin (F-actin) patches near the plasma membrane during adipogenesis. Depletion of Arp2/3 by knockdown of its subunits Arp3 or ARPC3 strongly impaired adipocyte differentiation, although adipogenesis-initiating factors were unaffected. Moreover, the assembly of F-actin-rich structures at the plasma membrane was suppressed and the cortical actin structure poorly developed after adipogenic induction in Arp2/3-deficient cells. Finally, we provide evidence that the cortical actin cytoskeleton is essential for efficient glucose transporter 4 (GLUT4) vesicle exocytosis and insulin signal transduction. These results show that the Arp2/3 complex is an essential regulator of adipocyte development through control of the formation of cortical actin structures, which may facilitate nutrient uptake and signalling events.</P>