MitoQ Alleviated PM2.5 Induced Pulmonary Epithelial Cells Injury by Inhibiting Mitochondrial-Mediated Apoptosis.

Background: Fine particulate matter (PM2.5), an important component of ambient air pollution, induces significant adverse health effects. MitoQuinone (MitoQ), a mitochondria-targeted antioxidant, has been reported to play a protective role in various diseases. However, the roles of MitoQ in PM2.5 induced pulmonary toxicity remains to be elucidated. Methods: All the experiments were performed at Higher Educational Key Laboratory for Translational Oncology of Fujian Province, Putian City, China in 2023. Pulmonary epithelial cells (A549) were pretreated with 4 µM MitoQ for 2 h and exposed to PM2.5 for 24 h. Cell viability was tested through CCK8 assay. Oxidative stress state and active mitochondria was used to study MitoQ's effect on PM2.5 induced injury, and cell apoptosis was measured using a flow cytometer and analyzed by Bcl-2 family. Results: MitoQ pretreatment significantly relieved a decreased cell viability, subsequently, MitoQ alleviated ROS production and prevented the reduction of T-AOC and GSH and increased the expression of NF-E2-related factor 2 (Nrf2) and p62 in A549 cells exposed to PM2.5. MitoQ restored the decreased mitochondrial dysfunction and dynamics disorder and inhibited activated mitochondrial-mediated apoptosis induced by PM2.5. Furthermore, the decreased ratio of Bcl-2/Bax and expression of Mcl-1 and the enhanced expression of Caspase-3 were reversed by MitoQ pretreatment. Conclusion: MitoQ might be regarded as a potential drug to relieve PM2.5 induced pulmonary epithelial cells damage.

Telephone follow-up by clinical pharmacists can improve treatment outcomes in patients with peptic ulcers: A prospective randomized study.

OBJECTIVE: The purpose of this study was to investigate the effect of pharmaceutical care by clinical pharmacists through telephone follow-up on the treatment outcomes in patients with peptic ulcers who had been discharged from the hospital. METHODS: A total of 120 patients with peptic ulcers discharged from the hospital were randomly divided into an intervention group and a control group, with 60 patients in each group. The patients in the two groups received different services. RESULTS: A total of 108 patients with peptic ulcers were enrolled in this study, including 53 in the intervention group and 55 in the control group. This study showed that the Helicobacter pylori eradication rate (19/23, 82.61% vs 13/29, 44.83%), awareness of peptic ulcer disease, medication compliance, diet compliance, and life compliance in the patients in the intervention group were higher than those in the patients in the control group. The H pylori eradication group had higher follow-up scores than the noneradication group. Sex and body mass index (BMI) did not affect the results in either group, but age did. In the control group, younger patients scored higher than older patients, whereas in the intervention group, this difference disappeared for diet compliance and life compliance, and significant differences remained for awareness of basic knowledge regarding peptic ulcer (AOKPU) and medication compliance. CONCLUSION: As a form of clinical pharmaceutical care, telephone follow-up by clinical pharmacists is recommended for discharged patients with peptic ulcers because it can improve treatment outcomes after discharge.

Importance of NUDT15 c.415C>T phenotype in treatment of inflammatory bowel disease with azathioprine and occurrence of severe myelosuppression: A case report.

Azathioprine is one of the main drugs in the treatment of inflammatory bowel disease (IBD). It has been widely used in the remission and maintenance treatment of IBD. Some patients may experience some degree of myelosuppression, but very few patients experience severe myelosuppression. Here, we report a 20-year-old male Asian patient with severe myelosuppression due to azathioprine treatment of IBD. In this case, the azathioprine-related genotyping test showed that homozygous wild-type TPMT*3 but a c.415C>T homozygous mutation was found in NUDT15. Our report strengthens the association between genetic polymorphisms of azathioprine-metabolizing enzymes and severe myelosuppression. Therefore, we recommend routine NUDT15 c.415C>T phenotype testing prior to long-term azathioprine treatment to avoid severe myelosuppression.