Treatment of gastric ulcer, traditional Chinese medicine may be a better choice.

ETHNOPHARMACOLOGICAL RELEVANCE: Gastric ulcer (GU) is the injury of the gastric mucosa caused by the stimulation of various pathogenic factors penetrating the deep mucosal muscle layer. An increasing number of studies have shown that traditional Chinese medicine (TCM) is highly effective in treating GU due to its multitarget, multilevel, and multi-pathway effects. AIM OF THE STUDY: To review the latest research progress in the treatment of GU by TCM, including clinical and experimental studies, focusing on the target and mechanism of action of drugs and providing a theoretical basis for the treatment of GU by natural herbs. MATERIALS AND METHODS: Electronic databases (PubMed, Elsevier, Springer, Web of Science, and CNKI) were searched using the keywords "gastric ulcer", "gastric mucosal lesion", "TCM" and or paired with "peptic ulcer" and "natural drugs" for studies published in the last fifteen years until 2023. RESULTS: TCM, including single components of natural products, Chinese patent medicines (CPM), and TCM decoction, is expected to treat GU by regulating various mechanisms, such as redox balance, inflammatory factors, angiogenesis, gastric mucosal protective factors, intestinal flora, apoptosis, and autophagy. CONCLUSIONS: We discussed and summarized the mechanism of TCM in the treatment of GU, which provided a sufficient basis for TCM treatment of GU.

Secreted Glycoproteins That Regulate Synaptic Function: the Dispatchers in the Central Nervous System.

Glycoproteins are proteins that contain oligosaccharide chains. As widely distributed functional proteins in the body, glycoproteins are essential for cellular development, cellular function maintenance, and intercellular communication. Glycoproteins not only play a role in the cell and the membrane, but they are also secreted in the intercell. These secreted glycoproteins are critical to the central nervous system for neurodevelopment and synaptic transmission. More specifically, secreted glycoproteins play indispensable roles in neurite growth mediation, axon guiding, synaptogenesis, neuronal differentiation, the release of synaptic vesicles, subunit composition of neurotransmitter receptors, and neurotransmitter receptor trafficking among other things. Abnormal expressions of secreted glycoproteins in the central nervous system are associated with abnormal neuron development, impaired synaptic organization/transmission, and neuropsychiatric disorders. This article reviews the secreted glycoproteins that regulate neuronal development and synaptic function in the central nervous system, and the molecular mechanism of these regulations, providing reference for research about synaptic function regulation and related central nervous system diseases.

The antiandrogenic effect of neferine, liensinine, and isoliensinine by inhibiting 5-α-reductase and androgen receptor expression via PI3K/AKT signaling pathway in prostate cancer.

Neferine, liensinine, and isoliensinine are bisbenzylisoquinoline alkaloids extracted from seed-embryos of Nelumbo nucifera Gaertn. In this study, we evaluated the anticancer activities and mechanism of action of these natural products in prostate cancer cells by MTT, wound healing, ELISA and Western blotting. Neferine, liensinine, and isoliensinine showed growth inhibition and displayed a significant anti-migration activity in prostate cancer cells. They induced apoptosis and autophagy by activating cleaved caspase-9, cleaved PAPR, Bax, LC3B-II, but decreased Bcl-2 and PARP protein expression in LNCaP cells 24 h after treatments. The apoptotic and cytotoxic effects of neferine, liensinine, and isoliensinine were significantly attenuated in the presence of the caspase inhibitor, Z-VAD-FMK. However, the effects were enhanced in the presence of Akt inhibitor (MK2206) and PI3K inhibitor (LY294002). Moreover, neferine, liensinine, and isoliensinine also downregulated the protein expression of androgen receptor, prostate-specific antigen, and type II 5-α-reductase. These results demonstrated that these bisbenzylisoquinoline alkaloids have the potential as promising therapeutics agents. They induced apoptosis via inactivation with the PI3K/AKT signal pathway.