Effects of 17β estradiol on blood pressure elevation in ovariectomized rats with collagen-induced arthritis via modulation of oxidative stress, inflammation, fibrosis, and apoptosis in the aorta involving TLR4/NOX4/NF-kβ and TGFβ1/fibronectin/α-SMA pathways.

Rheumatoid arthritis (RA) can cause blood pressure (BP) elevation in estrogen-deficient, post-menopausal women; however, the underlying mechanisms are not well understood. In this study, the aortic involvement and its underlying mechanisms that contribute to the BP elevation in estrogen-deficient, RA condition were identified. Ovariectomy was performed to create a state of estrogen deficiency and RA was then induced in ovariectomized rats by using incomplete Freund's adjuvant and immune-mediated collagen type-II.

Marine Cyanobacteria: A Rich Source of Structurally Unique Anti-Infectives for Drug Development.

Marine cyanobacteria represent a promising yet underexplored source of novel natural products with potent biological activities. Historically, the focus has been on isolating cytotoxic compounds from marine cyanobacteria, but a substantial number of these photosynthetic microorganisms also produce diverse specialized molecules with significant anti-infective properties. Given the global pressing need for new anti-infective lead compounds, this review provides a concise yet comprehensive overview of the current knowledge on anti-infective secondary metabolites derived from marine cyanobacteria.

Estrogen hindrance escalates inflammation and neurodegeneration in the hippocampal regions of collagen-induced arthritis female Sprague-Dawley rats.

This study aims to investigate the effect of estrogen hindrance, i.e., menopause in women for instance with rheumatoid arthritis on the brain hippocampal region by using collagen-induced arthritis (CIA) female rat model (RA).

Recent progress on small molecule TLR4 antagonist against triple-negative breast cancer progression and complications.

Toll-like receptor 4 (TLR4) plays a vital role in the innate immune response, but its overactivation has been associated with several diseases, such as aggressive progression of triple-negative breast cancer (TNBC). As a result, inhibiting TLR4 has emerged as a potential therapeutic strategy for this challenging breast cancer subtype. This review summarizes recent advancements in the development of small-molecule TLR4 antagonists to suppress TNBC growth, metastasis, and chemotherapy resistance.