1. siRNA Delivery for Control of Cyclin D1 and E2F1 Expression in Crohn’s DiseaseRusso I. et al. 2017. Transl Med UniSa. Jul; 17: 25–33.

One common feature of inflammatory bowel diseases (IBD) is an increased risk of developing colorectal cancer. The chronic inflammation of these diseases can interfere in the cellular cycle, leading the intestinal cells to duplicate uncontrollably what may end up generating a tumour.

Now, researchers have used siRNA molecules to reduce the production of cellular cycle proteins CyD1 and E2F1 in explanted intestinal tissue from Crohn’s disease patients. The siRNAs need to go inside the cells to make their effect but they can’t do it by themselves, so researchers used lipid nanocarriers to help the molecules cross the cellular membrane. As an outcome, researchers achieved a reduction of the amount of proteins related to intestinal cancer in the tissue. This shows the potential of nanocarriers in delivering siRNAs to prevent cancer progression in IBD.  To the publication>

2. Orally targeted galactosylated chitosan poly(lactic-co-glycolic acid) nanoparticles loaded with TNF-ɑ siRNA provide a novel strategy for the experimental treatment of ulcerative colitis. Huang Y. et al. 2018. Eur J Pharm Sci.

Inflammatory bowel diseases (IBD) are characterized by the excessive inflammation of the intestinal mucosa. Some current therapies use antibodies to target TNF-α, a proinflammatory protein released by macrophages, but exhibit serious side effects if they are supplied systemically. The use of siRNAs is a targeted alternative to silence TNF-α  and avoid these side effects. However, in order to reach the affected area and to enter the cells and make their effect.

To do this, researchers have engineered nanoparticles to carry the therapeutical siRNAs inside the macrophages. They coated the carriers with galactosylated chitosan, a molecule that help the nanocarriers cross the macrophage cellular membrane. Using this strategy, researchers have reduced the inflammation in the intestine of ulcerative colitis mice models. To the publication>