Introduction of diCN-substitution can lower the HOMO and improve the miscibility between diCN-USQ and PC71BM, leading to higher PCE.

Podocyte injury serves an important role during the progression of diabetic nephropathy (DN), and lycopene (Lyc) may display a potential protective effect against DN progression. The effects of Lyc on high glucose (HG)-induced podocyte apoptosis and the underlying mechanisms are not completely understood; therefore, the present study aimed to investigate the effects of Lyc on HG-induced MPC5 podocyte apoptosis and the underlying mechanism. In the present study, MPC5 podocytes were exposed to HG and different doses of Lyc. MPC5 podocyte viability and apoptosis were assessed by performing the MTT assay and flow cytometry, respectively. To explore the effects of Lyc on the PI3K/AKT signaling pathway and autophagy, LY294002 (LY) and 3-methyladenine (3-MA) were used as PI3K and autophagy inhibitors, respectively. The expression levels of nephrin, podocin, apoptosis-related proteins (Bax, Bcl-2 and cleaved caspase-3), autophagy-related proteins [Beclin-1 and microtubule associated protein 1 light chain 3 (LC3)II/LC3I] and certain key proteins involved in the PI3K/AKT signaling pathway were measured via western blotting. The results suggested that Lyc reversed the inhibitory effect of HG on cell viability, and the protein expression levels of nephrin and podocin, as well as the promoting effect of HG on MPC5 podocyte apoptosis. In addition, under HG conditions, Lyc upregulated the phosphorylation levels of PI3K and AKT, and reduced HG-and LY-mediated MPC5 podocyte apoptosis. Moreover, Lyc further increased HG-induced protein expression levels of Beclin-1 and LC3II/LC3I, and attenuated LY-mediated inhibition of HG-induced MPC5 podocyte autophagy. In addition, the effects of Lyc on HG-mediated MPC5 podocyte apoptosis were alleviated by 3-MA. Therefore, the present study suggested that Lyc may protect against HG-induced MPC5 podocyte apoptosis by promoting autophagy activity via activation of the PI3K/AKT signaling pathway.

Increasing life expectancy imposes big challenges to the global health of the male population, because some disorders, such as tumours, tend to progress with age (Bell et al., 2015). Among them, prostate cancer (PCa) is a leading cause of cancer-associated mortality among men, specifically in Western countries; the lowest rates of this cancer are seen in Africa and Asia. PCa has the highest heritability, accounting for almost 10% of all new male tumours. More than 650,000 men worldwide are diagnosed with PCa annually (Fitzpatrick et al., 2009). In addition to family history and genetic factors, well-established risk factors for PCa include Lynch syndrome, country of origin, age and race/ethnicity (Grönberg, 2003; Teoh et al., 2019). Today, PCa is diagnosed based on the measurement of serum prostate-specific antigen (PSA), also known as DRE (Misawa et al., 2017). PC3 is a grade IV PCa cell line that does not respond to fibroblast growth factors (FGF), androgens or glucocorticoids and has potential metastatic activity. It is useful in studying curative interventions in progressive PCa cells (Ashtiani et al., 2017). Understanding the molecular mechanisms correlated with PCa development and progression is pivotal, where long noncoding RNAs (lncRNAs) are hopeful candidates in assessing PCa initiation and tumorigenesis. Only a small portion of transcripts are translated into proteins, while the majority of them are noncoding RNAs (ncRNAs) (Bray

To investigate the mechanism of valsartan protecting podocytes and inhibiting renal injury in diabetic rats. The rat model of diabetic nephropathy was induced by combination of valsartan and high-sugar and high-fat diet. The urinary protein content, renal index, inflammatory and antioxidant indexes in the kidney, renal pathological changes and podocyte holes were investigated. Membrane WT1 and P-Cadherin protein expression levels. Compared with the model group, the 24h urine protein content of valsartan was significantly decreased (P<0.05). Valsartan significantly inhibited the body weight of the model group (P<0.01), and significantly inhibited The increase of renal index (P<0.05); the high and middle doses of valsartan could significantly reduce the levels of IL-β, TNF-α and IL-6 in rat kidney (P<0.05-0.01). The valsartan high and middle dose groups significantly reduced MDA content in rat kidney (P<0.05), and significantly increased SOD activity (P<0.05). HE and PAS staining showed that valsartan was used in model group rats. The pathological changes were alleviated, and the glomerular morphology returned to normal. The protein expression of WT1 and P-Cadherin in the kidney of DN rats by Western blot showed that Pin the kidney tissue of valsartan rats. The expression levels of Cadherin and WT1 protein were significantly increased (P<0.05). Valsartan can regulate the expression of podocyte membrane proteins WT1 and P-Cadherin to protect podocytes, and then repair renal function and anti-diabetic nephropathy.