Intergenerational toxic effects of parental exposure to [C mim]NO (n = 2,4,6) on nervous and skeletal development in zebrafish offspring.

Ionic liquids (ILs) are thought to have negative effects on human health. Researchers have explored the effects of ILs on zebrafish development during the early stages, but the intergenerational toxicity of ILs on zebrafish development has rarely been reported. Herein, parental zebrafish were exposed to different concentrations (0, 12.

The effects of ginsenoside Rb1 on fatty acid β-oxidation, mediated by AMPK, in the failing heart.

Objectives: This study intended to investigate the effects of on fatty acid β-oxidation (FAO) in rat failing heart and to identify potential mechanisms of improving heart failure (HF) by FAO pathway dependent on AMP-activated protein kinase (AMPK).

Materials And Methods: Rats with chronic HF, induced by adriamycin (), were randomly grouped into 7 groups. Gs-Rb1, adenine 9-β-D-arabinofuranoside (, specific AMPK inhibitor), and 5'-aminoimidazole-4-carboxamide riboside (, specific AMPK activator) were administered to rats with HF, singly and/or combinedly.

Ginsenoside Rb1 Ameliorates Autophagy of Hypoxia Cardiomyocytes from Neonatal Rats via AMP-Activated Protein Kinase Pathway.

Objective: To investigate whether ginsenoside-Rb1 (Gs-Rb1) improves the CoCl-induced autophagy of cardiomyocytes via upregulation of adenosine 5'-monophosphate-activated protein kinase (AMPK) pathway.

Methods: Ventricles from 1- to 3-day-old Wistar rats were sequentially digested, separated and incubated in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum for 3 days followed by synchronization. Neonatal rat cardiomyocytes were randomly divided into 7 groups: control group (normal level oxygen), hypoxia group (500 μmol/L CoCl), Gs-Rb1 group (200 μmol/L Gs-Rb1 + 500 μmol/L CoCl), Ara A group (500 μmol/L Ara A + 500 μmol/L CoCl), Ara A+ Gs-Rb1 group (500 μmol/L Ara A + 200 μmol/L Gs-Rb1 + 500 μmol/L CoCl), AICAR group [1 mmol/L 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) + 500 μmol/L CoCl], and AICAR+Gs-Rb1 group (1 mmol/L AICAR + 200 μmol/L Gs-Rb1 + 500 μmol/L CoCl).

Apelin-APJ effects of ginsenoside-Rb1 depending on hypoxia-induced factor 1α in hypoxia neonatal cardiomyocytes.

Objective: To investigate whether ginsenoside-Rb1 (Gs-Rb1) inhibits the apoptosis of hypoxia cardiomyocytes by up-regulating apelin-APJ system and whether the system is affected by hypoxia-induced factor 1α (Hif-1α).

Methods: Neonatal rat cardiomyocytes were randomly divided into 6 groups: a control group, a simple CoCl group, a simple Gs-Rb1 group, a CoCl and Gs-Rb1 hypoxia group, a CoCl and 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (YC-1) group, a CoCl and YC-1 group and a Gs-Rb1 group, in which YC-1 inhibits the synthesis and accelerates the degradation of Hif-1a. The concentration of CoCl, Gs-Rb1 and YC-1 was 500 μmol/L, 200 μmol/L and 5 μmol/L, respectively; the apoptosis ratio was analyzed with a flow cytometer; and apelin, APJ and Hif-1α were assayed with immunocytochemistry, Western blot assays and reverse transcription polymerase chain reaction (RT-PCR).

Ginsenoside Rb1 protects cardiomyocytes against CoCl2-induced apoptosis in neonatal rats by inhibiting mitochondria permeability transition pore opening.

Aim: To investigate whether mitochondria permeability transition pore (mPTP) opening was involved in ginsenoside Rb1 (Gs-Rb1) induced anti-hypoxia effects in neonatal rat cardiomyocytes ex vivo.

Methods: Cardiomyocytes were randomly divided into 7 groups: control group, hypoxia group (500 micromol/L CoCl(2)), Gs-Rb1 200 micromol/L group (CoCl(2) intervention+Gs-Rb1), wortmannin (PI3K inhibitor) 0.5 micromol/L group, wortmannin+Gs-Rb1 group, adenine 9-beta-D-arabinofuranoside (Ara A, AMPK inhibitor) 500 micromol/L group, and Ara A and Gs-Rb1 group.

Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardiomyocytes is mediated through the specific activation of glucose transporter-4 ex vivo.

Aim: The aim of this study was to investigate whether Gs-Rbl relieves the CoCl(2)-induced apoptosis of hypoxic neonatal rat cardiomyocytes and in which the role of glucose transporter-4 (GLUT-4).

Methods: Gs-Rbl (0, 10, 50, 100, 200, 400, and 500 micromol/L), adenine 9-beta-D-arabinofuranoside (ara A, 500 micromol/L; AMPK inhibitor) and wortmannin (0.5 micromol/L; PI3K inhibitor) only in combination with 200 micromol/L Gs-Rbl were administered in hypoxic cardiomyocytes, which were induced by 500 micromol/L CoCl(2) for 12 h.

[Influence of hypoxia on apoptosis and glucose intake in bone marrow derived mesenchymal stem cells in rats].

To investigate the effects of hypoxia on the apoptosis and glucose intake of mesenchymal stem cells (MSCs), MSCs derived from bone marrow of rats were incubated in the atmosphere of 1% O(2) for a series of time points and their glucose-intaking capacity, ultrastructural changes and apoptotic proportions were analyzed by (3)H-labeling assay, electron microscopy and flow cytometry, respectively. The results showed that the cultured cells took the fibroblast-like morphology and could be induced into osteoblasts and adipocytes under appropriate conditions. The proportions of apoptotic cells after hypoxia treatment for 1, 4 and 8 hours were 13.