2 research outputs found
<i>Cassia tora</i> Seed Extract and Its Active Compound Aurantio-obtusin Inhibit Allergic Responses in IgE-Mediated Mast Cells and Anaphylactic Models
<i>Cassia tora</i> seed
is widely used due to its various
biological properties including anticancer, antidiabetic, and anti-inflammatory
effects. However, there has been no report of the effects of <i>C. tora</i> seed extract (CTE) on immunoglobulin E (IgE)-mediated
allergic responses. In this research, we demonstrated the effects
of CTE and its active compound aurantio-obtusin on IgE-sensitized
allergic reactions in mast cells and passive cutaneous anaphylaxis
(PCA). CTE and aurantio-obtusin suppressed degranulation, histamine
production, and reactive oxygen species generation and inhibited the
production and mRNA expression of tumor necrosis factor-α and
interleukin-4. CTE and aurantio-obtusin also suppressed the prostaglandin
E<sub>2</sub> production and expression of cyclooxygenase 2. Furthermore,
CTE and aurantio-obtusin suppressed IgE-mediated FcεRI signaling
such as phosphorylation of Syk, protein kinase Cμ, phospholipase
Cγ, and extracellular signal-regulated kinases. CTE and aurantio-obtusin
blocked mast cell-dependent PCA in IgE-mediated mice. These results
suggest that CTE and aurantio-obtusin are a beneficial treatment for
allergy-related diseases
Gomisin J Inhibits Oleic Acid-Induced Hepatic Lipogenesis by Activation of the AMPK-Dependent Pathway and Inhibition of the Hepatokine Fetuin‑A in HepG2 Cells
The
aim of our study is to investigate the molecular mechanism
of gomisin J from Schisandra chinensis on the oleic acid (OA)-induced lipid accumulation in HepG2 cells.
Gomisin J attenuated lipid accumulation in OA-induced HepG2 cells.
It also suppressed the expression of lipogenic enzymes and inflammatory
mediators and increased the expression of lipolytic enzymes in OA-induced
HepG2 cells. Furthermore, the use of specific inhibitors and fetuin-A
siRNA and liver kinase B1 (LKB1) siRNA transfected cells demonstrated
that gomisin J regulated lipogenesis and lipolysis via inhibition
of fetuin-A and activation of an AMP-activated protein kinase (AMPK)-dependent
pathway in HepG2 cells. Our results showed that gomisin J suppressed
lipid accumulation by regulating the expression of lipogenic and lipolytic
enzymes and inflammatory molecules through activation of AMPK, LKB1,
and Ca<sup>2+</sup>/calmodulin-dependent protein kinase II and inhibition
of fetuin-A in HepG2 cells. This suggested that gomisin J has potential
benefits in treating nonalcoholic fatty liver disease