ABSTRACT
Objective: To explore the effect of Huangqisan on endoplasmic reticulum stress signaling pathway in liver tissues of high-fat diet-induced obese rats and its mechanisms. Method: Male SD rats were selected and fed with high-fat diet for 7 weeks continuously to establish an obese rat model. Then, the rats were randomly divided into model group, low and high-dose Huangqisan group (1.2, 2.4 g·kg-1), and Lipitor group (2 mg·kg-1), and orally administered with drugs for 15 consecutive weeks. The control group and the model group were perfused with the same volume of normal saline. The body weight, epididymal fat coefficient and liver coefficient of each group were determined separately. Fasting plasma glucose (FPG), total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) were determined by biochemical reagent method. The epididymal visceral adipose tissue and liver pathological changes were observed by hematoxylin and eosin (HE) staining. And the protein expression levels of sterol regulation element-binding transcription factor 1 (SREBP-1c), protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), inositol requiring enzyme 1 (IRE1α), p-inositol requiring enzyme 1 (p-IRE1α) in liver tissues were detected by Western blot methods. Result: Compared with the control group, the body weight, epididymal fat coefficient and liver coefficient of the model group were significantly increased(PPPα/p-IRE1α were increased(PPPPα/p-IRE1α protein expression levels to different degrees(PPConclusion: Huangqisan could regulate the glucose and lipid metabolism, alleviate liver pathology and reduce body weight, and its mechanism was probably related to reduction of SREBP-1c, PERK, IRE1α/p-IRE1α proteins expression levels.
ABSTRACT
Alzheimer's disease (AD) is a kind of neurodegenerative diseases, the most common cause of dementia. Although AD has been studied more than, 100 years and the Aβ and tau theory are most widely accepted among the theories achieved, yet it is not really clear what the mechanism related to AD works up to now. However, it is certain that AD is a kind of diseases resulting from multi-causes. Except for causes correlated with heredity, aging and life habits, environmental role is worth taking into consideration as well. Some metals, such as copper, aluminum, zinc and iron et al, can also have close relationship with AD. Now, we make an overview on the correlative researches in the field.
Subject(s)
Humans , Aluminum , Alzheimer Disease , Pathology , Copper , Iron , Metals , ZincABSTRACT
<p><b>AIM</b>To investigate the inhibition of amyloid beta-protein 42 (Abeta42) production in M146L cells by gamma-schisandrin.</p><p><b>METHODS</b>M146L cells which can produce considerable Abeta42 in vitro were treated with gamma-schisandrin (1.67, 5.00 and 15.00 microg x mL(-1)), beta-secretase inhibitor (S4562, 100.00 microg x mL(-1)) and gamma-secretase inhibitor (S2188, 13.68 microg x mL(-1)), separately. Cell counting kit-8 (CCK-8) was used to assess cell viability. Enzyme-linked immunosorbent assay (ELISA) was carried out to determine the amount of Abeta42. Western blotting was used to examine C99, an intermediary product of APP cleaved by beta-secretase. beta-Secretase and gamma-secretase activities were assayed by commercial kits.</p><p><b>RESULTS</b>The CCK-8 assay indicated that different concentrations of gamma-schisandrin had no neurotoxicity on the cultured M146L. And the ELISA test showed that the amount of Abeta42 secreted by M146L cells treated with gamma-schisandrin (5.00 and 15.00 microg x mL(-1)) decreased obviously as compared with solvent control. The results of Western blotting test indicated that there was no change of C99 contents and beta-secretase activity in gamma-schisandrin treated cells, while gamma-secretase activity decreased obviously.</p><p><b>CONCLUSION</b>gamma-Schisandrin inhibited production of Abeta42 in M146L cells through inhibiting gamma-secretase.</p>
Subject(s)
Animals , Cricetinae , Humans , Alzheimer Disease , Drug Therapy , Amyloid Precursor Protein Secretases , Metabolism , Amyloid beta-Peptides , CHO Cells , Cricetulus , Cyclooctanes , Dose-Response Relationship, Drug , Lignans , Peptide Fragments , Polycyclic Compounds , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of ginsenoside Rg1 on the influence of neprilysin expression induced by LPS in BT325 cell line.</p><p><b>METHOD</b>MTT was used to measure the levels of the survival rate of BT325 cultured with ginsenoside Rg1 and LPS in different concentrations. The expression of NEP was measured by RT-PCR.</p><p><b>RESULT</b>The survival rate of BT325 was obviously inhibited by LPS, and the expression of NEP was decreased. The survival rate of BT325 was obviously raised by ginsenoside Rg1, and the expression of NEP was increased.</p><p><b>CONCLUSION</b>LPS can cause cell damage, and decrease the expression of NEP. Ginsenoside Rg1 can exert neuroprotective properties which protects BT325 cell line from the cell toxicity of LPS.</p>
Subject(s)
Humans , Cell Line, Tumor , Cell Survival , Drugs, Chinese Herbal , Pharmacology , Ginsenosides , Pharmacology , Glioma , Metabolism , Pathology , Lipopolysaccharides , Neprilysin , Metabolism , Neuroprotective Agents , Pharmacology , Panax , Chemistry , Plants, Medicinal , ChemistryABSTRACT
The progress in the research of the chemical constituents and their pharmacological activities of Kadsura was summarized. These chemical constituents mainly contain lignanoids and triterpnoids, much of which are characteristic ingredients of the plant and have such activities as anti-oxidation, anti-HIV, and platelet active factor antagonists.