Corilagin alleviates radiation enteritis through caspase-1/gasdermin D-dependent pyroptosis by targeting aldo-keto reductase family 1 member C2 via glutathione metabolism.

Radiation enteritis, caused by radiation therapy for abdominopelvic malignancies, inhibits local tumor control and seriously affects the quality of life of patients. Therefore, effective strategies to mitigate radiation enteritis are urgently needed. Corilagin, a natural ellagitannin found in plants, exhibits antioxidant, anti-inflammatory, and antitumor effects.

RTA-408 overcomes cisplatin-resistant lung cancer by inhibiting WWP1-mediated NCOA4 ubiquitination to induce ferritinophagy and ferroptosis.

Worldwide, pulmonary carcinoma remains the predominant cause of cancer-induced fatalities. Cisplatin (DDP) is a platinum-containing cell cycle-non-specific chemotherapeutic agent and serves as the first-line treatment for non-small cell lung cancer (NSCLC). However, NSCLC cells gradually develop resistance to cisplatin during treatment, reducing drug sensitivity and leading to a significant decrease in the effect of chemotherapy or even treatment failure.

Golgicide A induces pyroptosis of lung cancer stem cells by regulating dTGN formation via GOLPH3/MYO18A complex.

Background: Lung cancer is a common malignant neoplasm, one of the leading causes of death worldwide. Cancer stem cells (CSCs) drive tumor recurrence, progression, and therapeutic resistance. Thus, targeting CSCs may contribute to lung cancer treatment and improve clinical outcomes.

Autophagy induced by PP121 alleviates MSU crystal-induced acute gouty arthritis via inhibition of the NLRP3 inflammasome.

Acute gouty arthritis (AGA) is a frequent self-limiting inflammatory condition produced by the deposition of monosodium urate (MSU) crystals in the joints and periarticular tissues of patients with hyperuricemia. However, no effective interventional measures currently exist for AGA. Pyroptosis, a kind of pro-inflammatory programmed cell death, plays a crucial role in MSU crystal-induced inflammation and represents a potential treatment target for AGA.

ATRA improves endothelial dysfunction in atherosclerotic rabbits by decreasing CAV‑1 expression and enhancing eNOS activity.

The aim of the present study was to explore the protective effects and possible mechanisms of all‑trans‑retinoic acid (ATRA) against atherosclerosis (AS). Rabbits were randomly allocated for standard or high‑fat diet with or without ATRA. After 12 weeks, the aortic rings of the rabbits were removed.

Myosin light chain kinase inhibitor ML7 improves vascular endothelial dysfunction via tight junction regulation in a rabbit model of atherosclerosis.

Vascular endothelial dysfunction (VED) is an important factor in the initiation and development of atherosclerosis (AS). Previous studies have demonstrated that endothelial permeability is increased in diet‑induced AS. However, the precise underlying mechanisms remain poorly understood.

Melatonin ameliorates vascular endothelial dysfunction, inflammation, and atherosclerosis by suppressing the TLR4/NF-κB system in high-fat-fed rabbits.

Vascular endothelial dysfunction (VED) and inflammation contribute to the initiation and progression of atherosclerosis. Melatonin (MLT) normalizes lipid profile, improves endothelial function, and possesses anti-inflammatory properties. However, the precise mechanisms are still unclear.

All-trans-retinoic acid ameliorated high fat diet-induced atherosclerosis in rabbits by inhibiting platelet activation and inflammation.

Background: All-trans-retinoic acid (atRA) is effective for many proliferative diseases. We investigated the protective effects of atRA against atherosclerosis.

Methods: Rabbits were randomly allocated to receive basal diet or an HFD for 4 weeks.