ABSTRACT
BACKGROUND: The role of primary-level medical pharmacists in medical institutions in China is limited; therefore, it is necessary to explore the role of pharmacists in the process of drug treatment. CASE SUMMARY: A Chinese pharmacist participated in the complete treatment of a patient with a duodenal ulcer. The rationale for drug treatment was evaluated, and adjustments were made to the antacid and anti-infective regimen, as well as the dose and frequency of administration. Body temperature, routine blood examination, and adverse drug reactions were strictly monitored. During treatment, the pharmacist recommended anti-infective therapy with ampicillin-sulbactam, which effectively controlled the infection. Additionally, the pharmacist suggested changing famotidine to lansoprazole for acid suppression and gastroprotective treatment, combined with Chinese patent medicine such as Kangfuxin Liquid. This is the first case report of a pharmacist in primary-level medical institutions adjusting drug use for patients with duodenal ulcer and pulmonary infection. CONCLUSION: A pharmacist participated in the treatment process, provided individualized medication adjustment, and achieved good clinical results.
ABSTRACT
Magnolol and honokiol are the two major active ingredients with similar structure and anticancer activity from traditional Chinese medicine Magnolia officinalis, and honokiol is now in a phase I clinical trial (CTR20170822) for advanced non-small cell lung cancer (NSCLC). In search of potent lead compounds with better activity, our previous study has demonstrated that magnolol derivative C2, 3-(4-aminopiperidin-1-yl)methyl magnolol, has better activity than honokiol. Here, based on the core of 3-(4-aminopiperidin-1-yl)methyl magnolol, we synthesized fifty-one magnolol derivatives. Among them, compound 30 exhibited the most potent antiproliferative activities on H460, HCC827, H1975 cell lines with the IC50 values of 0.63-0.93 µM, which were approximately 10- and 100-fold more potent than those of C2 and magnolol, respectively. Besides, oral administration of 30 and C2 on an H460 xenograft model also demonstrated that 30 has better activity than C2. Mechanism study revealed that 30 induced G0/G1 phase cell cycle arrest, apoptosis and autophagy in cancer cells. Moreover, blocking autophagy by the autophagic inhibitor enhanced the anticancer activity of 30in vitro and in vivo, suggesting autophagy played a cytoprotective role on 30-induced cancer cell death. Taken together, our study implied that compound 30 combined with autophagic inhibitor could be another choice for NSCLC treatment in further investigation.
