The SEPS1 -105G>A is associated with an increased risk of KBD and influences the expression of PI3K/Akt signaling pathway in KBD patients. Apoptosis induced by tBHP in chondrocyte might be mediated via up-regulation of PI3K/Akt, Na2SeO3 has an effect of anti-apoptosis by down-regulating of PI3K/Akt signaling pathway.

Emerging studies have proposed microRNAs (miRNAs) as novel therapeutic tools for cancer therapy. Nucleosome-binding protein 1 (NSBP1) has been suggested as an oncogene in various types of human cancers. The present study aimed to identify a novel miRNA that could directly target and negatively modulate NSBP1 expression. We found that NSBP1 was highly expressed in non‑small cell lung cancer (NSCLC) cells, and knockdown of NSBP1 by NSBP1 small interfering RNA (siRNA) significantly suppressed NSCLC cell proliferation and invasion. Bioinformatics analysis revealed that miR‑326 had a putative binding site within the 3'‑untranslated region of NSBP1. Their substantial relationship was further verified by dual‑luciferase reporter assay, real‑time quantitative polymerase chain reaction and western blot analysis. Overexpression of miR‑326 significantly inhibited NSCLC cell proliferation and invasion, which mimicked the effect of NSBP1 siRNA. Furthermore, suppression of NSBP1 by NSBP1 siRNA or miR‑326 overexpression remarkably repressed the expression of cyclin B1 and matrix metalloproteinase 9 (MMP9), which are associated with cancer cell proliferation and invasion. Moreover, overexpression of NSBP1 obviously abolished the inhibitory effect of miR‑326 on cyclin B1 and MMP9 expression. In addition, an inverse correlation between miR‑326 and NSBP1 expression levels was found in NSCLC clinical specimens. Our study demonstrated a direct target relationship between NSBP1 and miR‑326 through which miR‑326 inhibited cell proliferation and invasion of NSCLC cells. Thus, miR‑326‑NSBP1 is a promising candidate target for developing novel anticancer therapeutics for NSCLC.

Punicalagin (PG), a major bioactive ingredient in pomegranate juice, has been proven to have anti-oxidative stress properties and to exert protective effects on acute lung injuries induced by lipopolysaccharides. This study aimed to investigate the effects of PG treatment on hypoxic pulmonary hypertension (HPH) and the underlying mechanisms responsible for the effects. Rats were exposed to 10% oxygen for 2 wk (8 h/day) to induce the HPH model. PG (5, 15, 45[Formula: see text]mg/kg) was orally administered 10[Formula: see text]min before hypoxia each day. PG treatments at the doses of 15 and 45[Formula: see text]mg/kg/d decreased the mean pulmonary arterial pressure (mPAP) and alleviated right ventricular hypertrophy and vascular remodeling in HPH rats. Meanwhile, PG treatment attenuated the hypoxia-induced endothelial dysfunction of pulmonary artery rings. The beneficial effects of PG treatment were associated with improved nitric oxide (NO)-cGMP signaling and reduced oxidative stress, as evidenced by decreased superoxide generation, gp91[Formula: see text] expression and nitrotyrosine content in the pulmonary arteries. Furthermore, tempol's scavenging of oxidative stress also increased NO production and attenuated endothelial dysfunction and pulmonary hypertension in HPH rats. Combining tempol and PG did not exert additional beneficial effects compared to tempol alone. Our study indicated for the first time that PG treatment can protect against hypoxia-induced endothelial dysfunction and pulmonary hypertension in rats, which may be induced via its anti-oxidant actions.