Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.6.1.2 (
alanine aminotransferase
)
26,722
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The present study describes the antifungal potency of Nigella sativa seeds extract and the effect of immunomodulatory of N. sativa against aflatoxin- fed mice. Disc diffusion method was used for antifungal efficacy of aqueous extract of N. sativa. In animal experiments, lymphoid cell count, total and differential counts of PEC, the phagocytic activity of PEC and detection of the
plaque
-forming were determined. E-rosette-forming cells (RFC), T-cell mitogenesis assay cells,
ALT
and AST were detected. The aqueous extract of N. sativa (50%) exhibited high inhibition zone with most of isolates of R. stolonifera.The results indicated that treatment of mice by using N. sativa showed marked rise in the number of cells from thymus and PLN with dose 0.50 g and absolute number and comparative ratio of macrophages (P < 0.01) with the doses 0.40 and 0.50 g. There is gradually rise in the scavenger activity of PEC with the dose 0.50 g at 60 min. Serum level of
ALT
was markedly reduced with dose 0.50 g as compared with a control group. These results indicated that N. sativa is promising modifier of biological response.
...
PMID:Antifungal potency of Nigella sativa seeds extract against Rhizopus stolonifer and their effect of immunomodulatory against aflatoxin-fed mice. 3168 82
The purpose of the current study was to investigate the mechanism by which fisetin improves atherosclerosis (AS) by regulating lipid metabolism and senescence in apolipoprotein E-deficient (apoE
-/-
) mice. An AS model was established by feeding apoE
-/-
mice a high-fat diet. Mice were randomly divided into the model group (n=18), the fisetin group (n=18) and the atorvastatin group (n=18). The control group (n=18) was composed of wild-type C57BL/6 mice of the same age and genetic background. The fisetin and atorvastatin groups were respectively treated with aqueous solutions of fisetin (12.5 mg/kg) and atorvastatin (2 mg/kg) via oral gavage daily for 12 weeks. The pathological morphology, lipid accumulation, collagen deposition of the aortic sinus were observed, serum lipids, superoxide dismutase (SOD) and malondialdehyde (MDA) levels and
alanine aminotransferase
(
ALT
) and aspartate aminotransferase (AST) activities were measured in the peripheral blood serum. Additionally, the expressions of proprotein convertase subtilisin/kexin type 9 (PCSK9), lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), tumor suppressor protein p53 (p53), cyclin-dependent kinase inhibitor 1A (p21) and multiple tumor suppressor-1 (p16) were analyzed in the aorta. The results of the current study indicated that compared with the control group, a large area of AS
plaque
in the aortic sinus that contained a large amount of red-stained lipids and decreased collagen fiber content were found in the model group, which exhibited higher total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), oxidized low-density lipoprotein (ox-LDL) and MDA levels; higher
ALT
and AST activities, lower high-density lipoprotein cholesterol (HDL-C) and SOD levels and increased expression levels of PCSK9, LOX-1, p53, p21 and p16. Fisetin is a phytochemical and bioflavonoid that serves a potential role in chronic diseases including AS, obesity, diabetes and cancer due to its wide biological activities, such as regulating lipid metabolism and anti-aging, anti-oxidation and anti-inflammatory. Atorvastatin is recognized as a first-line treatment drug for AS; therefore it was used as a positive control in the current study. Following fisetin and atorvastatin treatment, both the AS
plaque
and the lipid accumulation in the aortic sinus were significantly reduced, and the expressions of PCSK9, LOX-1 and aging markers, including p53, p21 and p16 were downregulated.
...
PMID:Fisetin ameliorates atherosclerosis by regulating PCSK9 and LOX-1 in apoE
-/-
mice. 3326 11
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