Oral delivery of insulin via mesoporous carbon nanoparticles for colonic release allows glycemic control in diabetic rats

Haorong Lin,Jia Zhang,Chaochang Yu,Yan Lu,Jie Ning,Sixian Le,Yue Li,Lin‑quan Zang 한국탄소학회 2019 Carbon Letters Vol.29 No.2

In this article, a new type of mesoporous carbon nanoparticles (MCN) was fabricated as a potential oral delivery system of insulin to reduce the adverse reactions by hypodermic injection. The mesoporous carbon nanoparticles-carried insulin (MCNI) was studied using scanning electron microscopy (SEM), transmission electron microscopy (TEM), and Fourier transform infrared spectroscopy (FT-IR) compared with the blank MCNs. The Brunauer–Emmett–Teller (BET) method was utilized to calculate the specific surface area. The pore volume and pore size distribution (PSD) curves were calculated by Barrett–Joyner–Halenda (BJH) model. The entrapment efficiency (EE%) and loading content (LC%) of insulin onto the MCNs were determined by RP-HPLC. In vitro insulin release from MCNI was determined in simulated intestinal fluid. To evaluate the pharmacodynamics of MCNIs orally, the variation of glycemia of diabetic rats after oral administration of MCNIs was compared with the rats receiving hypodermic injection of insulin. Besides, the absorption of FITC-labeled MCNs in HCT-116 cells was tested. The results showed that there is significant difference between MCNs and MCNIs through SEM, TEM, and FT-IR. The entrapment efficiency, loading content and in vitro insulin release met the requirements of the pharmacodynamic study. The specific surface area, pore volume and pore size of MCNIs were significantly decreased compared to that of MCNs. The pharmacodynamics study showed that the blood sugar level was significantly decreased after the oral administration of MCNIs. The FITC-labeled MCNs showed significant absorption in HCT-116 cells. The MCNIs were successfully synthesized with commendable entrapment efficiency and loading content which preferably decreased the blood sugar in diabetes rats via oral administration.

Diacylglycerol acyltransferase 1 (DGAT1) inhibition by furofuran lignans from stems of Acanthopanax senticosus

BanBan Li,Jia Lin Li,Na Li,Shi-Zhou Qi,이현선,Le Zhang,Shan-Shan Xing,Zhen Dong Tuo,Long Cui 대한약학회 2017 Archives of Pharmacal Research Vol.40 No.11

Two new furofuran lignans were isolated fromthe stems of Acanthopanax senticosus, along with sevenknown compounds. Their structures were all determined byspectroscopic analyses and chemical methods. All theisolates were evaluated for in vitro inhibitory activityagainst DGAT1 and DGAT2. Compounds 1 and 2 werefound to exhibit selective inhibitory activity on DGAT1with IC50 values 89.5 ± 1.5 and 57.5 ± 1.3 lM,respectively.

Recombinant Human Thioredoxin-1 Protects Macrophages from Oxidized Low-Density Lipoprotein-Induced Foam Cell Formation and Cell Apoptosis

Zhang, Hui,Liu, Qi,Lin, Jia-Le,Wang, Yu,Zhang, Ruo-Xi,Hou, Jing-Bo,Yu, Bo The Korean Society of Applied Pharmacology 2018 Biomolecules & Therapeutics(구 응용약물학회지) Vol.26 No.2

Oxidized low-density lipoprotein (ox-LDL)-induced macrophage foam cell formation and apoptosis play critical roles in the pathogenesis of atherosclerosis. Thioredoxin-1 (Trx) is an antioxidant that potently protects various cells from oxidative stress-induced cell death. However, the protective effect of Trx on ox-LDL-induced macrophage foam cell formation and apoptosis has not been studied. This study aims to investigate the effect of recombinant human Trx (rhTrx) on ox-LDL-stimulated RAW264.7 macrophages and elucidate the possible mechanisms. RhTrx significantly inhibited ox-LDL-induced cholesterol accumulation and apoptosis in RAW264.7 macrophages. RhTrx also suppressed the ox-LDL-induced overproduction of lectin-like oxidized LDL receptor (LOX-1), Bax and activated caspase-3, but it increased the expression of Bcl-2. In addition, rhTrx markedly inhibited the ox-LDL-induced production of intracellular reactive oxygen species (ROS) and phosphorylation of p38 mitogen-activated protein kinases (MAPK). Furthermore, anisomycin (a p38 MAPK activator) abolished the protective effect of rhTrx on ox-LDL-stimulated RAW264.7 cells, and SB203580 (a p38 MAPK inhibitor) exerted a similar effect as rhTrx. Collectively, these findings indicate that rhTrx suppresses ox-LDL-stimulated foam cell formation and macrophage apoptosis by inhibiting ROS generation, p38 MAPK activation and LOX-1 expression. Therefore, we propose that rhTrx has therapeutic potential in the prevention and treatment of atherosclerosis.

Recombinant Human Thioredoxin-1 Protects Macrophages from Oxidized Low-Density Lipoprotein-Induced Foam Cell Formation and Cell Apoptosis

( Hui Zhang ),( Qi Liu ),( Jia-le Lin ),( Yu Wang ),( Ruo-xi Zhang ),( Jing-bo Hou ),( Bo Yu ) 한국응용약물학회 2018 Biomolecules & Therapeutics(구 응용약물학회지) Vol.26 No.2

Oxidized low-density lipoprotein (ox-LDL)-induced macrophage foam cell formation and apoptosis play critical roles in the pathogenesis of atherosclerosis. Thioredoxin-1 (Trx) is an antioxidant that potently protects various cells from oxidative stress-induced cell death. However, the protective effect of Trx on ox-LDL-induced macrophage foam cell formation and apoptosis has not been studied. This study aims to investigate the effect of recombinant human Trx (rhTrx) on ox-LDL-stimulated RAW264.7 macrophages and elucidate the possible mechanisms. RhTrx significantly inhibited ox-LDL-induced cholesterol accumulation and apoptosis in RAW264.7 macrophages. RhTrx also suppressed the ox-LDL-induced overproduction of lectin-like oxidized LDL receptor (LOX- 1), Bax and activated caspase-3, but it increased the expression of Bcl-2. In addition, rhTrx markedly inhibited the ox-LDL-induced production of intracellular reactive oxygen species (ROS) and phosphorylation of p38 mitogen-activated protein kinases (MAPK). Furthermore, anisomycin (a p38 MAPK activator) abolished the protective effect of rhTrx on ox-LDL-stimulated RAW264.7 cells, and SB203580 (a p38 MAPK inhibitor) exerted a similar effect as rhTrx. Collectively, these findings indicate that rhTrx suppresses ox-LDL-stimulated foam cell formation and macrophage apoptosis by inhibiting ROS generation, p38 MAPK activation and LOX-1 expression. Therefore, we propose that rhTrx has therapeutic potential in the prevention and treatment of atherosclerosis.

Establishing a Nomogram for Stage IA-IIB Cervical Cancer Patients after Complete Resection

Zhou, Hang,Li, Xiong,Zhang, Yuan,Jia, Yao,Hu, Ting,Yang, Ru,Huang, Ke-Cheng,Chen, Zhi-Lan,Wang, Shao-Shuai,Tang, Fang-Xu,Zhou, Jin,Chen, Yi-Le,Wu, Li,Han, Xiao-Bing,Lin, Zhong-Qiu,Lu, Xiao-Mei,Xing, H Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.9

Background: This study aimed to establish a nomogram by combining clinicopathologic factors with overall survival of stage IA-IIB cervical cancer patients after complete resection with pelvic lymphadenectomy. Materials and Methods: This nomogram was based on a retrospective study on 1,563 stage IA-IIB cervical cancer patients who underwent complete resection and lymphadenectomy from 2002 to 2008. The nomogram was constructed based on multivariate analysis using Cox proportional hazard regression. The accuracy and discriminative ability of the nomogram were measured by concordance index (C-index) and calibration curve. Results: Multivariate analysis identified lymph node metastasis (LNM), lymph-vascular space invasion (LVSI), stromal invasion, parametrial invasion, tumor diameter and histology as independent prognostic factors associated with cervical cancer survival. These factors were selected for construction of the nomogram. The C-index of the nomogram was 0.71 (95% CI, 0.65 to 0.77), and calibration of the nomogram showed good agreement between the 5-year predicted survival and the actual observation. Conclusions: We developed a nomogram predicting 5-year overall survival of surgically treated stage IA-IIB cervical cancer patients. More comprehensive information that is provided by this nomogram could provide further insight into personalized therapy selection.

A Novel Distributed Equivalent Circuit Model for Single-Core Cables

Li Rui-Fang,Hu Hao,Cao Xiao-Bin,Li Zhong-Mei,Li Jun-Hao,Zhu Chuan-Lin,Liu Le-Jia 대한전기학회 2024 Journal of Electrical Engineering & Technology Vol.19 No.1

The number of cables used for urban power supply increases rapidly. The sheath current in these cables, which is generated via induction, produces a current loss. When the situation is serious, the ground lead and the middle connector of the cable will be burned. In this paper, the existing single-core cable equivalent circuit model is used to calculate the sheath current of a 3-phase cable under the condition of non-transposition and cross connection. By comparing the calculated results with the simulation and the experimental results, it is found that the current distribution law for the sheath, which was obtained using the existing model, difers substantially from both the simulation and actual measurements. The error reason of the existing model is revealed, and it is found that the magnitude and phase of the current in the metal sheath of the cable varies with the position under the combined efect of distributed capacitances in the cable and the core-current fux, especially for a 3-phase cross connection, each section of the cable does not meet Kirchhof’s laws, but the sheath electric current in the existing models are considered equal everywhere. Therefore, a novel cable equivalent model is proposed in this paper, which is based on a distributed circuit, and an equation to calculate the sheath current is derived. The model presented in this paper corrects the problems of the existing model, which can be applied to power system, subway, high-speed rail, and any application of single-core cables.