Ferroptosis: The Entanglement between Traditional Drugs and Nanodrugs in Tumor Therapy.

Ferroptosis is a non-apoptotic programmed cell death caused by the accumulation of lipid peroxide. System Xc-/glutathione peroxidase 4 (GPX4) axis and iron axis are two main pathways regulating ferroptosis. Simultaneously, multiple pathways are also involved in the ferroptosis regulation. Ferroptosis is an intense area of the current study. With the improvement of the regulatory mechanisms that underlie ferroptosis, a variety of drugs associated with ferroptosis have been discovered and developed for cancer therapy. Among them, traditional drugs were developed initially. Small molecule compounds that regulate ferroptosis signaling pathway and iron complexes that promote the Fenton reaction have become important drugs for inducing ferroptosis. In recent years, the emerging development of nanotechnology has promoted the research of ferroptosis nanodrugs. Iron-based nanomaterials are extensively tested as ferroptosis-inducing agents. Furthermore, nanoscale drug delivery systems offer a suitable scaffold for traditional drug therapies. Traditional drugs and nanodrugs are complementary, each with their own strengths and limitations. This review describes the latest studies on the regulation of ferroptosis in tumor cells and focuses on the entanglement between traditional drugs and nanodrugs. To conclude, the challenges and perspectives in this field are put forward.

Strontium-Incorporated Carbon Nitride Nanosheets Modulate Intracellular Tension for Reinforced Bone Regeneration.

Strontium-containing agents have been demonstrated to elicit both bone anabolic and antiosteoporotic effects, showing great potential for the treatment of bone loss. However, an increased incidence of strontium-induced side effects restricts their clinical applications. Herein, oxidized carbon nitride nanosheets (CN) are delicately used to incorporate Sr2+ for the first time to achieve high osteogenic efficacy. The lamellar structure and enriched nitrogen species of CN provide them with a high surface area-to-volume ratio and abundant anchoring sites for Sr2+ incorporation. Importantly, Sr2+-incorporated CN (CNS) could synergistically promote osteoblast differentiation and bone regeneration at a single, very low Sr2+ dose. Mechanically, CNS could activate the FAK/RhoA signaling pathway to modulate the intracellular tension that stimulates osteoblasts differentiation. The present study will provide a new paradigm to enhance the efficacy of osteogenic metal ions by using lamellar nanocarriers.

[Mechanism studies on hepatotoxicity of rats induced by fructus toosendan].

OBJECTIVE: To study the effects on SOD, MDA, gamma-GT, GSH-Px and inflammatory factor (TNF-alpha, NF-kappaB, ICAM-1) in rats that induced by fructus toosendan, and to search for the hepatotoxicity mechanism of rats that induced by fructus toosendan. METHOD: The SD rats were given fructus toosendan 120 g x kg(-1) by orally for 45 days, then take the liver tissue of control and fructus toosendan group to prepare liver homogenate. The activities of SOD, the content of MDA, the ratio of SOD and MDA, the content of gamma-GT and glutathione peroxidase (GSH-Px) were detected according to the methods of kit. The tumor necosis factor-alpha (TNF-alpha) was detected by ABC-ELISA. The expression of NF-kappaB p65 and ICAM-1 were detected by immunohistochemistry. RESULT: The rats were given fructus toosendan 120 g x kg(-1) by orally for 45days, the SOD and GSH-Px activities in liver tissue decreased, the content of MDA increased, the ratio of SOD and MDA decreased, the content of gamma-GT and TNF-alpha, the masculine expression of NF-kappaB p65 and ICAM-1 increased. CONCLUSION: After the rats were given fructus toosendan, the liver can be damaged obviously, and the mechanism of hepatotoxicity perhaps related to free radical and inflammatory factor.