Molecular Mechanisms of Gynostemma pentaphyllum in Prevention and Treatment of Non-Small-Cell Lung Cancer: Objective. Lung cancer represents the leading cause of cancer death on a global scale. Gynostemma pentaphyllum (G. pentaphyllum), a traditional medicinal material with a high medicinal and health value, has recently been reported for its anticancer activity. However, the pharmacological mechanism of G. pentaphyllum in non-small-cell lung cancer (NSCLC) remains to be elucidated. Methods. The active ingredients of G. pentaphyllum were obtained from the TCMSP database and known therapeutic targets of NSCLC from the GeneCards and OMIM databases. Disease-drug common targets are subjected to protein-protein interaction (PPI), GO enrichment analysis, and KEGG pathway enrichment analysis. A molecular docking strategy was performed to verify the interaction between molecules. Results. We found a total of 24 compounds of G. pentaphyllum fulfilling OB30 concomitant with DL0.18 and corresponding 81 target genes in the TCMSP database, with 5062 NSCLC-related genes collected in the GeneCards and OMIM databases. The network consisting of the disease-target compound was obtained, including 8 active ingredients and 69 common targets. The PPI network with 65 nodes and 645 edges was visualized. After functional enrichment analysis, it was revealed that the therapeutic effects of G. pentaphyllum on NSCLC were achieved through response to ketone, gland development, and cellular response to xenobiotic stimulus. After molecular docking analysis, it was revealed that the two active ingredients of G. pentaphyllum, quercetin and rhamnazin, bound well and stably to their targets (MYC, ESR1, and HIF1A). Conclusion. Our study, based on network pharmacology, identifies active ingredients, targets, and pathways model mechanism of G. pentaphyllum when it is used to treat NSCLC.

Approximately 5-10% of all cancer types are hereditary cancer syndromes, which are caused by pathogenic mutations in cancer susceptibility genes. In this investigation, a hereditary cancer pedigree was collected from a province in southern China, and the proband was a 31-year-old woman with breast cancer. Utilizing blood whole exome sequencing technology and bioinformatics analysis, the sole heterozygous missense mutation in PIBF1 that exhibits trait segregation was identified: PIBF1 (p.R405Q). The pedigree also included two other mutations that may be linked to carcinogenesis: RAD51D (p.K91Ifs*13) and BRCA2 (p.G3134Afs*29). This research concentrated on PIBF1 (p.R405Q) and employed breast cancer as a tumor model. In vitro and in vivo experiments showed that PIBF1-WT suppressed breast cancer cell proliferation, colony formation, invasive ability, and tumorigenesis. However, PIBF1 (p.R405Q) attenuated or inhibited the function of PIBF1-WT. Mechanistically, PIBF1-WT resisted cisplatin-induced DNA damage, significantly down-regulated the expression of γ-H2AX, and affected DNA damage repair, thus exerting a cancer inhibitory function. Interestingly, PIBF1 (p.R405Q) affects protein stability, thereby mitigating or eliminating the inhibitory effect of PIBF1. Furthermore, this family's polygenic risk factors for cancer are analyzed, and there is speculation about potential synergistic effects between PIBF1 and DNA damage repair genes like BRCA2 and RAD51D. In conclusion, PIBF1 regulates the cell cycle and DNA damage repair, PIBF1(p.R405Q) increases susceptibility to cancer, multiple DNA damage repair gene mutations may synergistically promote cancer progression in this cancer family lineage, and PIBF1(p.R405Q) may be one of the polygenic risk factors for familial hereditary cancer syndromes.

Objective: Effects of sevoflurane and propofol anesthesia on cardioprotective and postoperative recovery were compared in patients with off-pump coronary bypass surgery. Methods: Preoperative and postoperative myocardial enzymes, other blood biochemical indexes and clinical outcome were retrospectively analyzed. Results: Compared with the propofol group, the serum concentration of troponin I (1.19 ± 2.68 ng/mL vs 0.24 ± 0.52 ng/mL, p=0.018) and the brain natriuretic peptide (713.19 ± 849.31 pg/dL vs 403.78 ± 237.23 pg/dL, p=0.017) were significantly lower in sevoflurane group, the postoperative clinical outcome was not significantly different between the two groups. Conclusion: Sevoflurane was used for anesthesia maintenance could reduce the serum level of cTnI and BNP after off-pump coronary bypass surgery, but the values of clinical outcome were limited.