Sacran, a type of new sulfated polysaccharide, is a biomaterial with
excellent water solubility and safety, and is expected to be used in
pharmaceuticals of the future. In the present study,
sacran suppressed oxidative stress and inhibited the progression of chronic
kidney disease (CKD). Sacran also had a multifaceted effect on the progression
of CKD by altering the mix of intestinal microflora as a prebiotic in addition
to the above effects. Thus, sacran is expected to have an effective
nephroprotective effect especially when oxidative stress initially appears at
the early stage of renal failure.
Hepatocellular carcinoma is one of the most frequent
cancers. Sinomenine (SIN) is a compound derived from Sinomenium
acutum. Authors’ investigations have found that SIN suppressed SK-Hep-1
cells’ proliferation, enhanced the collapse of potential of the mitochondrial
membrane, triggered cell apoptosis, down-regulated PI3K p85α, AKT1, BCL-2,
Pro-Caspase 9, Pro-Caspase 3 expressions, and up-regulated Cleaved Caspase 9
and Cleaved Caspase 3 expressions. In addition, insulin-like growth factor-1 could reverse the high
apoptosis of SK-Hep-1 cells induced by SIN. Therefore, authors revealed that inhibition
of PI3K/AKT1 signaling cascade by SIN induced hepatocellular carcinoma cells
apoptosis.
Atrial
enlargement often provides arrhythmogenic substrates, leading to the induction of
atrial fibrillation. The
authors examined the
anatomical, molecular biological, and
electrophysiological characteristics of remodeled atria in rats with 8- and
12-week of aorto-venocaval shunt
(AVS). It is noteworthy that marked electrophysiological changes were detected
only in the AVS-12W rat despite obvious increments in atrial and ventricular
tissue weights and altered gene expression in the AVS-8W rat, which suggests
that the electrical remodeling observed in the atrium is preceded by structural
remodeling after AVS surgery. These findings provide important information on experimental evidence regarding
the timing of generation of arrhythmogenic substrate in the atria.
Breast cancer are originated from cancer
stem cells (CSCs), which contribute to drug resistance and recurrence. The
authors examined
the effects of transforming growth factor beta (TGFβ) signaling on
proliferation of breast CSCs. TGFβ induced the proliferation of CSCs via
phosphorylation of sphingosine kinase 1 (SphK1) via a Smad-independent manner
and subsequent production of sphingosine-1-phosphate (S1P). Moreover, Notch
pathway was involved in the S1P response via S1P receptor 3. These results suggest
that TGFβ-SphK1-S1P-Notch signaling pathway is a novel therapeutic target in
breast cancer.
Hepatic stellate cells (HSCs) are a key
player in the pathogenesis of hepatic fibrosis including cirrhosis. The
development of hepatic fibrosis is associated with enhanced calcium signaling in
HSCs. However, the regulatory mechanism of calcium signaling in HSCs is largely
unknown. In addition, there is no specific therapeutic drug for hepatic
fibrosis currently. This report reveals that calcium-sensing receptors are
expressed in human HSCs and function in the regulation of calcium signaling and
cell proliferation. These findings help to elucidate the molecular mechanism of
hepatic fibrosis and develop a potential therapeutic target for hepatic
fibrosis.