Atherosclerosis is a pathological condition of the accumulation of fat in the arteries, leading to cardiovascular disorders. Atherosclerosis management remains a challenge and conventional medicines are used for the management of the company has several limitations. This study evaluated the effects of tabersonine protection against atherosclerosis and rated the molecular mechanisms of action.Atherosclerosis induced by feeding the apolipoprotein E (ApoE) -deficient mice a high-fat diet. Mice treated with 20 or 40 mg / kg intraperitoneally tabersonine for 12 weeks of the study. Atherosclerosis markers and nitric oxide are measured in the serum of ApoE-deficient mice. Inflammatory mediators and markers of oxidative stress were assessed using enzyme-linked immunosorbent assay tests.
Western blotting, reverse transcriptase quantitative polymerase chain reaction and immunohistochemistry analyzes were performed to determine the expression of proteins in tissue.The tabersonine-treatment group aorta had improved lipid profile and liver function improved, compared with the group treated ApoE. tabersonine treatment resulted in decreased levels of nitric oxide, cytokines, and oxidative stress, compared with ApoE.
Change expression levels of protein inhibitor activated Stat3 (PIAS3), signal transducer and activator of transcription-3 (STAT-3), and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα) in ApoE mice -deficient tabersonine are helped by treatment. In addition, cAMP-response-element-binding (CREB) expression increased in aortic tissue tabersonine treatment group, compared with ApoE group.These results suggest tabersonine which ameliorates expression of Stat3 by activating CREB protein in atherosclerotic ApoE-deficient mice.
Activation of CREB Protein With Tabersonine Attenuates STAT3 During Atherosclerosis in Apolipoprotein E-Deficient Mice.
Dimethyl fumarate relieve nitroglycerin (NTG) -induced migraine in rats.
Oxidative stress and inflammatory pathways involved in migraine and endogenous antioxidant defense system have a role in hyperalgesia in migraine prevention. In this study, we aimed to evaluate the role of the molecules of the most pharmacologically effective between the ester of fumaric acid (FAEs), fumaric dimethyl, nuclear factor E2-related factor 2 / response element antioxidants (NRF-2 / ARE) pathway-mediated, in regulating hypersensitivity in a mouse model of nitroglycerin (NTG) -induced migraine.Mice administered orally with DMF at a dose of 10, 30, and 100 mg / kg, 5 minutes after intraperitoneal injection of NTG.
We did histological and molecular analysis throughout the brain and behavioral tests after 4 hours with NTG-induced migraine. The expression of nuclear factor kappa-light-chain-enhancer activated B cells (NF-кB) subunit p65, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (IκBα), nitric oxide synthase (iNOS), cyclooxygenase 2 (COX- 2), NRF-2, manganese superoxide dismutase (Mn-SOD), and heme oxygenase – 1 (HO-1) was detected by Western blot.
Description: This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease.
Description: A polyclonal antibody against Phospho-FOS (S32). Recognizes Phospho-FOS (S32) from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: WB, ELISA;WB:1/500-1/2000.ELISA:1/5000
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human Phospho-BAD(S32) . This antibody is tested and proven to work in the following applications:
Description: A polyclonal antibody against Phospho-NFKBIA (S32/S36). Recognizes Phospho-NFKBIA (S32/S36) from Human, Mouse, Rat, Monkey. This antibody is Unconjugated. Tested in the following application: WB, IHC, IF, ELISA;WB:1/500-1/2000.IHC:1/100-1/300.IF:1/200-1/1000.ELISA:1/10000
Description: This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease.
Description: Histones are basic nuclear proteins that are responsible for the nucleosome structure of the chromosomal fiber in eukaryotes. Two molecules of each of the four core histones (H2A, H2B, H3, and H4) form an octamer, around which approximately 146 bp of DNA is wrapped in repeating units, called nucleosomes. The linker histone, H1, interacts with linker DNA between nucleosomes and functions in the compaction of chromatin into higher order structures. This gene contains introns and its mRNA is polyadenylated, unlike most histone genes. The protein encoded is a replication-independent member of the histone H3 family.
Description: IkappaB‚Äêalpha is a protein encoded by the NFKBIA gene which is approximately 35,6 kDa. IkappaB‚Äêalpha is localised to the cytoplasm and nucleus. It is involved in activated TLR4 signalling, 4-1BB pathway and toll-like receptor signalling pathways. It inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL dimers in the cytoplasm through masking of their nuclear localization signals. IkappaB‚Äêalpha is expressed in adherent monocytes. Mutations in the NFKBIA gene may result in ectodermal dysplasia with T-cell immunodeficiency. STJ90311 is a synthesized peptide derived from human IkappaB-alpha around the phosphorylation site of S32/S36. This primary antibody specifically binds to endogenous IkappaB‚Äêalpha protein which only binds about S23/36 when S23/36 is phosphorylated.
Cardboard freezer box, hinged lid, insert for 36 screw-cap 5ml tubes, 5.25 x 5.25 x 3 inches
The tail of the film, hot plate, orofacial formalin, and photophobia tests used to evaluate migraine-like pain and light sensitivity associated with migraine. In addition, we evaluated the NRF-2-dependent mechanism in vitro stimulation of the trigeminal ganglia cells extracted by dietilenatriamina / nitric oxide (DETA / NO), nitric oxide (NO) donor. Cells pre-treated with DMF and antagonists of NRF-2, trigonelline (TR) 2 hours before treatment DETA / NO stimulation.DMF particularly reducing histological damage as shown by cresyl violet staining; Also, set both NF-kB and NRF-2 pathway, DMF treatment reduce the severity of inflammation and boost protective antioxidant action
