ABSTRACT
To investigate the impact of the ethanoic fractions of Periploca forrestii Schltr. (P. forrestii) in ameliorating the liver injury caused by fluoride ingestion and to explore the potential mechanisms. Initially, an in vitro fluorosis cell model was constructed using the human normal liver cell line (L-02) induced by fluoride. Cell viability was assessed using the CCK-8 assay kit. The lactate dehydrogenase (LDH) assay kit was utilized to measure LDH content in the cell supernatant, while the malonic dialdehyde (MDA) assay kit was employed to determine MDA levels within the cells. Subsequently, a fluorosis rat model was established, and LDH content in the cell supernatant was measured using the LDH assay kit. Various parameters, including MDA, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and reactive oxygen species (ROS) content within the cells, were detected using appropriate assay kits. Additionally, cell apoptosis rate was determined using the Annexin V-FITC/PI cell apoptosis assay kit. The protein expression levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase-3, Cleaved Caspase-3, Caspase-9, and Cleaved Caspase-9 were analyzed through Western blotting. Compared to the model group, the ethanolic fraction D of P.forrestii (Fr.D) increased cell viability (P < 0.01) and decreased LDH and MDA levels (P < 0.01). In the high-dose Fr.D treatment group of fluoride-poisoned rats, serum ALT, AST, LDH and MDA levels significantly decreased (P < 0.01). Results from rat primary cells exhibited that the Fr.D administration group exhibited significantly higher cell survival rates than the fluoride group (P < 0.01). Similarly, primary rat cells treated with Fr.D showed enhanced cell viability (P < 0.05) and reduced apoptosis rate, LDH, MDA, SOD, GSH-Px, CAT, and ROS levels (P < 0.05) compared to the model group. Western blot analysis indicated that the Fr.D treatment group elevated the Bcl-2/Bax protein expression ratio and reduced Caspase-3 and Caspase-9 activation levels (P < 0.01) compared to the model group. The results suggest that components within the Fr.D from Periploca forrestii may alleviate fluoride-induced liver injury by potentially counteracting oxidative stress and cell apoptosis.
Subject(s)
Periploca , Rats , Humans , Animals , Reactive Oxygen Species/metabolism , Caspase 3/metabolism , Caspase 9/metabolism , Fluorides/toxicity , Fluorides/metabolism , Liver/metabolism , Apoptosis , Proto-Oncogene Proteins c-bcl-2/metabolism , Superoxide Dismutase/metabolism , Oxidative StressABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression of angiotensin converting enzyme 2 (ACE2) and the changes treated with angiotensin converting enzyme inhibitor (ACEI), and its signal transduction pathway.</p><p><b>METHODS</b>Atrial tissues were obtained from 47 patients with RHD undergoing cardiac surgery. The mRNA of ACE2 and ACE were semi-qualified by RT-PCR and normalized to the gene beta-actin. Western blot analysis was employed to examine the expressions of ACE2, ACE, ERK1/2 and phosphorylated ERK (pERK1/2). The atrial tissue angiotensin II (Ang II) content was determined by radioimmunoassay detection.</p><p><b>RESULTS</b>The expression of ACE2 was significantly decreased (P < 0.05), the expression of ACE and pERK1/2 were significantly increased (P < 0.05), and the level of atrial tissue Ang II was significantly increased in patients with chronic atrial fibrillation group (CAF) compared with sinus rhythm group (SR) (P < 0.05). Compared with CAF patients treated without ACEI, the expression of ACE2 significantly increased (P < 0.01), and the relative activity of ERK1/2 significantly decreased (P < 0.05), whereas the expression of ACE and the level of atrial tissue Ang II remained unchanged in CAF patients treated with ACEI.</p><p><b>CONCLUSIONS</b>The study suggested that the dysequilibrium of ACE/ACE2 might play an important role in the process of atrial fibrillation, which may be related to the activation of ERK1/2 pathway. The clinical effect of long-term treatment of ACEI maybe associated with elevated ACE2 expression but not ACE expression.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Angiotensin-Converting Enzyme Inhibitors , Therapeutic Uses , Atrial Fibrillation , Drug Therapy , Metabolism , Heart Atria , Metabolism , Mitogen-Activated Protein Kinase 1 , Metabolism , Mitogen-Activated Protein Kinase 3 , Metabolism , Peptidyl-Dipeptidase A , Metabolism , RNA, Messenger , Metabolism , Signal TransductionABSTRACT
<p><b>OBJECTIVE</b>To evaluate serum-vascular endothelial growth factor (S-VEGF) in the differentiation of solitary pulmonary nodule (SPN).</p><p><b>METHODS</b>Serum level of VEGF of 68 patients with SPN was measured by ELISA kit, and compared with the control group of 20 normal subjects. The nodules were diagnosed by operation and pathology.</p><p><b>RESULTS</b>The median level of S-VEGF was 42.5 (range from 10 to 170) pg/ml in the control, 44 (range from 18 to 360) pg/ml in benign nodule group and 75 (range from 18 to 890) pg/ml in lung cancer group, with significant difference observed between the nodule group and control (P < 0.01), and between the lung cancer group and the benign nodule group (P < 0.05), but not between the benign nodule group and the control. In addition, when S-VEGF in different pathologic types of the limited number of lung cancer patients were compared, no significant difference was observed.</p><p><b>CONCLUSION</b>S-VEGF is valuable in the differential diagnosis of solitary pulmonary nodule. An elevated S-VEGF level >or= 100 pg/ml in patients with SPN may strongly speak for a malignant nodule. Operation is suggested.</p>
