Brassaiopsis glomerulata (Blum) Regel (B.glomerulata) is recognized as a traditional Chinese medicine (TCM) primarily used for promoting blood circulation and removing stasis. It is frequently utilized in the treatment of injuries resulting from falls and bumps. Despite its effective use in clinical treatment for ischemic stroke (IS), there are currently no reports on its composition and mechanism of action, which affects its promotion. The study investigated the chemical components and molecular mechanisms of B.glomerulata, with the following components: UPLC-Q-TOF-MS, network pharmacology Analysis and experimental verification in vivo and vitro. The effect of B.glomerulata on interfering with ischemic stroke was assessed on MCAO/R rats and ORD cell model. Then the compositional analysis was conducted using UPLC-Q-TOF-MS. Furthermore, network pharmacology and molecular docking techniques were explored to identify potential targets and pathways. The predicted mechanisms of action were ultimately confirmed by immunohistochemistry and protein blotting. B. glomerulata exhibited neuroprotective effects in MCAO/R rats by reductions in hippocampal and cortical neuronal damage, brain infarction, and cerebral edema. Both in vivo and in vitro experiments demonstrated that it decreased ROS and MDA levels, increased SOD and GSH levels, thereby inhibiting oxidative stress. Moreover, the improvements in neuronal morphology and the modulation of Nissl bodies suggested a potential mechanism underlying its neuroprotective action. Additionally, B.glomerulata exhibited concentration-dependent reductions in Bax and Caspase-3 expressions, along with increases in GFAP, Bcl2/Bax ratio, p-PI3K, p-AKT, and p-mTOR levels. B.glomerulata exhibited neuroprotective effects against cerebral ischemia-reperfusion injury both in vivo and in vitro. It prevented oxidative stress damage and inhibited apoptosis of ischemic stroke through the PI3K/AKT/mTOR pathway.

Glioblastoma (GBM) is an aggressive and highly malignant primary brain tumour, accounting for a significant proportion of adult brain tumours. It is associated with a poor prognosis and high recurrence rates. Although temozolomide (TMZ) remains the standard first‐line chemotherapy for GBM, its clinical efficacy is often limited by the development of drug resistance and toxic effects on normal tissues. Melatonin (Mel), a natural indoleamine synthesised by the pineal gland, has demonstrated synergistic anti‐tumour effects when combined with various chemotherapy agents in multiple studies. This study investigates the synergistic potential of Mel to enhance TMZ's therapeutic efficacy against GBM. The results demonstrate that the combination of Mel and TMZ significantly inhibits glioblastoma cell proliferation, migration, and invasion. Mechanistically, this synergistic effect is mediated through the NF‐κB/COX‐2 signalling pathway. Mel enhances TMZ's anti‐tumour activity by inhibiting IκBα phosphorylation, suppressing NF‐κB activation, and downregulating COX‐2 expression. Additionally, the combination treatment induced apoptosis via activation of the Caspase‐3 pathway. These results suggest that Mel can potentiate the therapeutic efficacy of TMZ in glioblastoma treatment, offering a promising strategy to overcome TMZ resistance while reducing its associated toxicity.

Organic cation transporter member 2 (OCT2) is an N‑glycosylated transporter that has been shown to be closely associated with the transport of antitumor drugs. Oxaliplatin, a platinum‑based drug, is used for the chemotherapy of colorectal cancer (CRC). However, oxaliplatin resistance is a major challenge in the treatment of advanced CRC. The aim of the present study was to better understand the mechanism underlying the chemosensitivity of CRC cells to oxaliplatin. The present study describes a potential novel strategy for enhancing oxaliplatin sensitivity involving the glycosylation of this drug transporter, specifically the modification of β‑1,6‑N‑acetylglucosamine (GlcNAc) residues by N‑acetylglucosaminyltransferase V (GnT‑V). The results revealed that the downregulation of GnT‑V inhibited the oxaliplatin chemosensitivity of CW‑2 cells. Furthermore, the knockdown of GnT‑V caused a marked reduction in the presence of β‑1,6‑GlcNAc structures on OCT2 and decreased the localization of OCT2 in the cytomembrane, which were associated with a reduced uptake of oxaliplatin in wild‑type and oxaliplatin‑resistant CW‑2 cells. Overall, the study provides novel insights into the molecular mechanism by which GnT‑V regulates the chemosensitivity to oxaliplatin, which involves the modulation of the drug transporter OCT2 by N‑glycosylation in CRC cells.

In this study, we aimed to find the targets of resveratrol in nasopharyngeal carcinoma (NPC) by network target prediction and investigate the possible mechanisms through experimental verification. Firstly, resveratrol and NPC-specific targets were combined with protein-protein interactions to construct a systematical resveratrol targets-NPC network. Consistently, molecular docking was performed to predict the molecular determinants of resveratrol against NPC. In order to clarify this point, the anti-cancer effects of resveratrol were investigated in the CNE2 cell lines in vitro and NPC cases in vivo. Functional enrichment results suggested that resveratrol played anti-NPC role mainly through MAPK pathway and the potential targets were MAPK1, MAPK3, STAT3, TP53, PIK3CA, PIK3R1, SRC, MAPK8, RELA and VEGFA. In vitro, resveratrol inhibited proliferation, invasion, migration and eventually induced apoptosis in CNE2 cells on time-and dose-dependent manner. Meanwhile, western blot confirmed that resveratrol exerted apoptotic activity of NPC cells by inhibiting MAPK cell signaling activation. Clinically, Immuno-histochemical staining showed significant differential p-ERK1/2, p-JNK and p-P38 activation between tumor-surrounding and NPC cases. Altogether, our findings identified resveratrol could play potent inhibition and apoptosis on human NPC cells possibly by targeting MAPK pathways and suggested that resveratrol had the potential to be an effective bioactive compound in NPC patients.