NF-κB pathway as a molecular target for curcumin in diabetes mellitus treatment: Focusing on oxidative stress and inflammation.

Diabetes mellitus (DM) is a collection of metabolic disorder that is characterized by chronic hyperglycemia. Recent studies have demonstrated the crucial involvement of oxidative stress (OS) and inflammatory reactions in the development of DM. Curcumin (CUR), a natural compound derived from turmeric, exerts beneficial effects on diabetes mellitus through its interaction with the nuclear factor kappa B (NF-κB) pathway. Research indicates that CUR targets inflammatory mediators in diabetes, including tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6), by modulating the NF-κB signaling pathway. By reducing the expression of these inflammatory factors, CUR demonstrates protective effects in DM by improving pancreatic ß-cells function, normalizing inflammatory cytokines, reducing OS and enhancing insulin sensitivity. The findings reveal that CUR administration effectively lowered blood glucose elevation, reinstated diminished serum insulin levels, and enhanced body weight in Streptozotocin -induced diabetic rats. CUR exerts its beneficial effects in management of diabetic complications through regulation of signaling pathways, such as calcium-calmodulin (CaM)-dependent protein kinase II (CaMKII), peroxisome proliferator-activated receptor gamma (PPAR-γ), NF-κB, and transforming growth factor ß1 (TGFB1). Moreover, CUR reversed the heightened expression of inflammatory cytokines (TNF-α, Interleukin-1 beta (IL-1ß), IL-6) and chemokines like MCP-1 in diabetic specimens, vindicating its anti-inflammatory potency in counteracting hyperglycemia-induced alterations. CUR diminishes OS, avert structural kidney damage linked to diabetic nephropathy, and suppress NF-κB activity. Furthermore, CUR exhibited a protective effect against diabetic cardiomyopathy, lung injury, and diabetic gastroparesis. Conclusively, the study posits that CUR could potentially offer therapeutic benefits in relieving diabetic complications through its influence on the NF-κB pathway.

A comprehensive view on the quercetin impact on bladder cancer: Focusing on oxidative stress, cellular, and molecular mechanisms.

Bladder cancer (BC) is known as a prevalent genitourinary malignancy and has a significant mortality rate worldwide. Despite recent therapeutic approaches, the recurrence rate is high, highlighting the need for a new strategy to reduce the BC cell progression. Quercetin, a flavonoid compound, demonstrated promising anticancer properties and could be used in the management of various malignancies such as BC. This comprehensive review summarized quercetin's cellular and molecular mechanisms underlying anticancer activities. The study's findings indicated that quercetin prevents the proliferation of the human BC cell line, promotes apoptosis of BIU-87 cells, reduces the expression of p-P70S6K, and induces apoptosis by p-AMPK. Moreover, quercetin restricts tumor growth through the AMPK/mTOR cascade and prevents colony formation of human BC cells by triggering DNA damage. Studying this review article will help researchers better understand quercetin's functional role in the prevention and treatment of BC.