OBJECTIVE:To explore the role of clinical pharmacists on pharmaceutical care for allergic reaction caused by ox-aliplatin. METHODS:Clinical pharmacists conducted pharmaceutical care for a patient with oxaliplatin-induced allergic reaction, and suggested stopping taking oxaliplatin,giving Dexamethasone injection 5 mg and then slowing down injection speed. RE-SULTS:Physicians adopted the suggestions of clinical pharmacists. Allergic reaction relieved 5 min after giving Dexamethasone in-jection. The patient didn't suffered from this allergic reaction again under tight supervision. CONCLUSIONS:Oxaliplatin is often used for tumor therapy. Medical staff should be familiar with the prevention,diagnosis and treatment of ADR,evaluate oxaliplatin chemotherapy plan in advance and screen high risk allergy factor. The participation of clinical pharmacists in pharmaceutical care contribute to ADR monitoring and promote safe and rational drug use in the clinic.

Objective To investigate the selective killing effect of MDA/IL-24 on human hepatocellular carcinoma line HepG2 in vitro and provide a theoretical basis for gene therapy of hepatocellular carcinoma.Methods The MDA-7/IL-24 gene was transfected into human hepatocullular carcinoma cell line HepG2 and normal liver cell line L02 with a replication-incompetent adenovirus vector.The mRNA and protein expression of MDA7/IL-24 in HepG2 and L02 cells was examined by RT-PCR and ELISA assay respectively.MTT assay and flow cytometry were used to study tumor cell proliferation and cell cycle in vitro.Hoechst and Annexin-V and PI staining were studied to indicate the apoptosis.Results RT-PCR confirmed that the exogenous MDA-7/IL-24 gene was expressed in HepG2 and L02 cells.The protein product was confirmed by assay of the supernatant with ELISA.MTT and apoptosis test indicated MDA-7/IL-24 induced growth suppression and cell apoptosis of the HepG2 cell in vitro but not in cell line L02,and cell cycle test revealed MDA-7/IL-24 could block HepG2 cell in G2/M but not in L02.Conclusions MDA-7/IL-24 selectively induces growth suppression and apoptosis in lines HepG2 in vitro but not in L02 cell,which indicates that adenovirus mediated MDA-7/IL-24 can be an excellent tool for gene therapy in hepatocellular carcinoma.

Lipotoxicity is a pivotal factor that initiates and exacerbates liver injury and is involved in the development of metabolic-associated fatty liver disease (MAFLD). However, there are few reported lipotoxicity inhibitors. Here, we identified a natural anti-lipotoxicity candidate, HN-001, from the marine fungus Aspergillus sp. C1. HN-001 dose- and time- dependently reversed palmitic acid (PA)-induced hepatocyte death. This protection was associated with IRE-1α-mediated XBP-1 splicing inhibition, which resulted in suppression of XBP-1s nuclear translocation and transcriptional regulation. Knockdown of XBP-1s attenuated lipotoxicity, but no additional ameliorative effect of HN-001 on lipotoxicity was observed in XBP-1s knockdown hepatocytes. Notably, the ER stress and lipotoxicity amelioration was associated with PLA2. Both HN-001 and the PLA2 inhibitor MAFP inhibited PLA2 activity, reduced lysophosphatidylcholine (LPC) level, subsequently ameliorated lipotoxicity. In contrast, overexpression of PLA2 caused exacerbation of lipotoxicity and weakened the anti-lipotoxic effects of HN-001. Additionally, HN-001 treatment suppressed the downstream pro-apoptotic JNK pathway. In vivo, chronic administration of HN-001 (i.p.) in mice alleviated all manifestations of MAFLD, including hepatic steatosis, liver injury, inflammation, and fibrogenesis. These effects were correlated with PLA2/IRE-1α/XBP-1s axis and JNK signaling suppression. These data indicate that HN-001 has therapeutic potential for MAFLD because it suppresses lipotoxicity, and provide a natural structural basis for developing anti-MAFLD candidates.