Nanocurcumin

A rheumatic condition characterized by inflammation and increased bone mass at the primary sites of inflammation is called ankylosing spondylitis (AS). The pathophysiology of AS has been linked to Th17 and Regulatory T (Treg) cells, as well as the immunological and miRNA variables that are associated with them. This study looked at how immunological and miRNA variables in AS patients' peripheral blood (PB) were affected by nanocurcumin.

For four months, 30 patients with AS were part of the test group, who got nanocurcumin daily, and 30 patients in the control group, who received a placebo. Using flow cytometry, the frequency of Th17 and Treg was determined. Real-time polymerase chain reaction was used to measure the expression levels of HIF1A, various related microRNAs (miRNAs; miR-18a, miR-206, and miR-30a), and CD39 with CD73 in Patients PBMCs. An enzyme-linked immunosorbent assay was also used to measure the amounts of factors and cytokines secreted in serum.

Following treatment with nanocurcumin, patients with AS experienced a large rise in Treg cells and a decrease in Th17 cells. The RT-PCR results showed that while miR-18a was dramatically upregulated after nanocurcumin treatment, the expression of miR-206 and miR-30a was significantly downregulated. Additionally, compared to the control group, the nanocurcumin-treated group had lower levels of HIF-1alpha production and higher levels of IGF-1, TGF-β, CD39, and CD73.

According to the findings, Th17 and Treg cell dysregulation, along with other immunological factors and miRNAs in PB, affects the progression of AS. Nanocurcumin therapy has the potential to control these variables, as well as Th17 and Treg cells, and may, therefore, help treat AS and other autoimmune disorders.

Breast cancer (BC) is one of the most prevalent malignant tumors among women, with estrogen receptor (ER)-positive patients constituting approximately 70 % of all cases. Endocrine therapy is currently a treatment option for patients with ER-positive BC; however, the development of resistance significantly limits the effectiveness of this treatment. Nano-curcumin (Nano-CUR) possesses anticancer properties and enhances bioavailability by improving the hydrophobic character of curcumin (CUR). However, the underlying mechanism by which Nano-CUR affects tamoxifen (TAM) resistance in ER-positive BC remains unknown. Here, we found that Nano-CUR promoted apoptosis and cell cycle arrest, inhibited cell proliferation and reduced the levels of cancer stem cells (CSCs)-related markers, including octamer-binding protein (OCT4), Nanog homeobox (NANOG) and sex-determining region Y-box 2 (SOX2) in TAM-resistant BC cells. Additionally, Nano-CUR demonstrated the ability to inhibit tumor malignant progression in TAM-treated BC mice. Mechanistically, Nano-CUR blocked the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in MCF-7/TAM and T47D/TAM cells. The activation of this pathway by its activators (PI3K activator 740Y-P, AKT activator SC-79, and mTOR activator MHY1485) effectively alleviated the anti-tumor effect induced by Nano-CUR in TAM-resistant BC cells. Collectively, these findings reveal that Nano-CUR contributes to the reduction of tumorigenesis and TAM resistance in ER-positive BC cells by inhibiting the PI3K/AKT/mTOR signaling pathway.