Institution
Liaoning University of Traditional Chinese Medicine
Education•Shenyang, China•
About: Liaoning University of Traditional Chinese Medicine is a education organization based out in Shenyang, China. It is known for research contribution in the topics: Randomized controlled trial & Acupuncture. The organization has 2040 authors who have published 1326 publications receiving 14664 citations.
Topics: Randomized controlled trial, Acupuncture, Apoptosis, Cancer, Portulaca
Papers published on a yearly basis
Papers
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TL;DR: Two new esters identified as 1-ethyl 7-(4-octyl-5-oxocyclopenta-1,3-dien-1-yl) heptanedioate (1) and ethyl (7E,9E)-6-oxooctadeca-7,9-diamoate (2) were isolated from the aerial parts of Portulaca oleracea L. as discussed by the authors.
7 citations
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22 Mar 2021TL;DR: In this paper, Tanshinone IIA (TIIA) combined with cyclosporine A (CsA) pretreatment was used to alleviate myocardial cell apoptosis induced by renal ischemia-reperfusion (IR), and to determine whether TIIA combined with CsA would attenuate myocardious cells apoptosis by modulating mitochondrial function through the PI3K/Akt/Bad pathway in obese rats.
Abstract: Acute myocardial injury (AMI), which is induced by renal ischemia-reperfusion (IR), is a significant cause of acute kidney injury (AKI)-related associated death. Obesity increases the severity and frequency of AMI and AKI. Tanshinone IIA (TIIA) combined with cyclosporine A (CsA) pretreatment was used to alleviate myocardial cell apoptosis induced by renal IR, and to determine whether TIIA combined with CsA would attenuate myocardial cell apoptosis by modulating mitochondrial function through the PI3K/Akt/Bad pathway in obese rats. Male rates were fed a high fat diet for 8 weeks to generate obesity. AKI was induced by 30 min of kidney ischemia followed 24 h of reperfusion. Obese rats were given TIIA (10 mg/kg·d) for 2 weeks and CsA (5 mg/kg) 30 min before renal IR. After 24 h of reperfusion, the rats were anaesthetized, the blood were fetched from the abdominal aorta and kidney were fetched from abdominal cavity, then related indicators were examined. TIIA combined with CsA can alleviate the pathohistological injury and apoptosis induced by renal IR in myocardial cells. TIIA combined with CsA improved cardiac function after renal ischemia (30 min)-reperfusion (24 h) in obese rats. At the same time, TIIA combined with CsA improved mitochondrial function. Abnormal function of mitochondria was supported by decreases in respiration controlling rate (RCR), intracellular adenosine triphosphate (ATP), oxygen consumption rate, and mitochondrial membrane potential (MMP), and increases in mitochondrial reactive oxygen species (ROS), opening of the mitochondrial permeability transition pore (mPTP), mitochondrial DNA damage, and mitochondrial respiratory chain complex enzymes. The injury of mitochondrial dynamic function was assessed by decrease in dynamin-related protein 1 (Drp1), and increases in mitofusin1/2 (Mfn1/2), and mitochondrial biogenesis injury was assessed by decreases in PPARγ coactivator-1-α (PGC-1), nucleo respiratory factor1 (Nrf1), and transcription factor A of mitochondrial (TFam). We used isolated mitochondria from rat myocardial tissues to demonstrate that myocardial mitochondrial dysfunction occurred along with renal IR to induce myocardial cell apoptosis; obesity aggravated apoptosis. TIIA combined with CsA attenuated myocardial cell apoptosis by modulating mitochondrial function through the PI3K/Akt/Bad pathway in obese rats.
7 citations
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TL;DR: In vivo and in vitro experiments indicated that HA/CPP modified paclitaxel plus tetrandrine micelles could be selectively accumulated into tumour sites and exhibited the strong antitumor activity with negligible toxicity, suggesting that HA-PEG2000-CPP modifications might provide a new strategy for treating gastric cancer.
Abstract: Gastric cancer is a malignant tumour characterised by the uncontrolled cell growth. The incidence and mortality of gastric cancer remain high for the invasion and metastasis. We are urgently seekin...
7 citations
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TL;DR: It is demonstrated that estradiol enhanced osteogenic differentiation of rBMSCs and that the c-Jun N-terminal kinase (JNK) signaling pathway was involved in this process, providing insights into the molecular mechanisms involved in rB MSC osteogenesis upon est radiol stimulation.
Abstract: Bone marrow stromal cells (BMSCs) can differentiate into osteoblasts. The present study investigated the osteogenic effects of estradiol, as well as the role of the c‑Jun N‑terminal kinase (JNK) signaling pathway in promoting estradiol‑enhanced osteogenesis of rat (r)BMSCs. rBMSCs were treated for 7 days with or without estradiol and further treated with or without the JNK‑specific inhibitor SP600125. The role of estrogen during rBMSC osteogenesis was evaluated by alkaline phosphatase activity and mineralized nodule formation using the Gomori method and Alizarin red S staining, respectively. Subsequently, the mRNA expression levels of transforming growth factor-β1 (TGF‑β1) and core‑binding factor α1 (Cbfα1) were evaluated by reverse transcription‑quantitative polymerase chain reaction, and TGF‑β1, Cbfα1 and phosphorylated (p)‑JNK protein expression was detected by western blotting. All groups treated with SP600125 expressed low levels of TGF‑β1 and Cbfα1 mRNA and protein, and low p‑JNK protein expression. Compared with the control cells, rBMSCs cultured with estradiol exhibited a significant upregulation in the expression levels of osteogenic genes and proteins. The present study demonstrated that estradiol enhanced osteogenic differentiation of rBMSCs and that the JNK signaling pathway was involved in this process, providing insights into the molecular mechanisms involved in rBMSC osteogenesis upon estradiol stimulation.
7 citations
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TL;DR: Eupatilin showed poor absorption, extensive metabolism into E‐7‐G and a wide tissue distribution, especially in the intestine, and these pharmacokinetic results yield helpful insights into the pharmacological actions of eup atilin.
7 citations
Authors
Showing all 2045 results
Name | H-index | Papers | Citations |
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Hang Xiao | 64 | 618 | 16026 |
Muhammad Riaz | 58 | 934 | 15927 |
Jianping Liu | 45 | 333 | 7977 |
Guoan Luo | 45 | 221 | 6358 |
Xingshun Qi | 40 | 308 | 5409 |
Mei Wang | 29 | 201 | 6007 |
Xiaozhong Guo | 28 | 142 | 2269 |
Zhiwei Cao | 27 | 110 | 2879 |
Xinggang Yang | 26 | 113 | 2292 |
Ruixin Zhu | 25 | 110 | 2119 |
Ran Wang | 23 | 157 | 1942 |
Li-Ping Bai | 22 | 95 | 1824 |
Ke Liu | 19 | 31 | 1183 |
Ahmed M. Metwaly | 17 | 51 | 682 |
Kailin Tang | 17 | 40 | 919 |