Although carbon monoxide (CO)-based treatments have demonstrated the high cancer efficacy by promoting mitochondrial damage and core-region penetrating ability, the efficiency was often compromised by protective autophagy (mitophagy). Herein, cannabidiol (CBD) is integrated into biomimetic carbon monoxide nanocomplexes (HMPOC@M) to address this issue by inducing excessive autophagy. The biomimetic membrane not only prevents premature drugs leakage, but also prolongs blood circulation for tumor enrichment. After entering the acidic tumor microenvironment, carbon monoxide (CO) donors are stimulated by hydrogen oxide (H₂O₂) to disintegrate into CO and Mn²⁺. The comprehensive effect of CO/Mn²⁺ and CBD can induce ROS-mediated cell apoptosis. In addition, HMPOC@M-mediated excessive autophagy can promote cancer cell death by increasing autophagic flux via class III PI3K/BECN1 complex activation and blocking autolysosome degradation via LAMP1 downregulation. Furthermore, in vivo experiments showed that HMPOC@M+ laser strongly inhibited tumor growth and attenuated liver and lung metastases by downregulating VEGF and MMP9 proteins. This strategy may highlight the pro-death role of excessive autophagy in TNBC treatment, providing a novel yet versatile avenue to enhance the efficacy of CO treatments. Importantly, this work also indicated the applicability of CBD for triple-negative breast cancer (TNBC) therapy through excessive autophagy.

Objective To investigate the role of clinical pharmacists in identifying adverse drug reactions (ADR), to draw clinical attention to the possibility of drug-induced lung injury caused by rhG-CSF, and distinguish them from infectious diseases. Methods A case of rhG-CSF induced acute lung injury was analyzed. After analyzing the relationship between rhG-CSF and acute eosinophilic pneumonia, exploring the possible mechanism, in combination with the patient's condition, the clinical pharmacist put forward the suggestion for the treatment of the disease. Results After receiving rhG-CSF, the patient's eosinophils increased, the pneumonia was aggravated, and the effect of anti-infection treatment was poor. Eosinophils pneumonia associated with rhG-CSF was considered. The patient's pulmonary symptoms improved after treatment with glucocorticoid in combination with withdrawal of antibiotics and antiviral drugs, and eosinophil returned to normal. Conclusion rhG- can cause rare eosinophilic pneumonia. The clinical pharmacist's participation in clinical treatment can help to identify drug-induced diseases, reorient the direction of treatment and ensure the success of clinical therapy.