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Rheumatoid arthritis (RA) is a widespread autoimmune inflammatory disease. It implicates damage to bones, cartilage, and joints with uncertain pathogenesis. It is coupled with an elevated risk of cardiovascular complications and human disability. The conventional dosage forms for RA treatment pose numerous problems including poor efficacy, large dosages, frequent administration, limited responsiveness, greater expenses, and severe side effects. The nanoparticulate systems are emerging as a new thought for the diagnosis and treatment of RA. Anti-inflammatory drug-loaded nanoparticulate systems aid in the active and passive targeting of the inflamed region. Improved bioavailability and targetability are achieved by using these systems. In this review, the pathophysiology of RA and its conventional treatment has been discussed. The role of various nanoparticulate systems for passive and active targeting of RA has been reviewed. The authors have summarized the current practices in the typical and novel nanosystems to improve the quality of life in RA patients.

The transforming growth factor-β (TGF-β) signaling pathway exhibits an important role in cancer invasion and metastasis. Excessive expression of TGF-β activates Smad4, leading to the upregulation of downstream metastasis-associated genes. Thus, the inhibition of the TGF-β/Smad4 signaling pathway may be a novel strategy for treatment of cancer metastasis. Baicalein, a flavonoid derived from the root of Scutellaria baicalensis, has been reported to exert strong anti-tumor activity towards various types of cancer. In the present study the effect of baicalein on migration and invasion of cancer cells was evaluated using wound-healing and Transwell assays. In order to investigate the possible molecular mechanisms of the anti-metastatic effects of baicalein, quantitative polymerase chain reaction (qPCR) and western blot analyses were performed to examine the effect on the expression of TGF‑β, Smad4, N-cadherin, vimentin, ZEB1 and ZEB2. It was determined that baicalein inhibited the migration and invasion of AGS cells by suppressing the TGF-β/Smad4 signaling pathway. In addition, baicalein treatment reduced the expression of the metastasis-associated N-cadherin, vimentin, ZEB1 and ZEB2, downstream target genes of the TGF‑β/Smad4 signaling pathway. Collectively, these results suggest that inhibition of the metastasis of cancer cells via inactivation of TGF-β/Smad4 signaling is one of the mechanisms by which baicalein may treat cancer.