A series of novel N-(2-arylethyl) isoquinoline derivatives were designed, synthesized and evaluated for their anti-cancer activities. Among these analogs, compound 9a exhibited the potential anti-cancer activities on HepG2 and HCT116 cells with IC50 values of 2.52 and 1.99 microg x mL(-1), respectively. Cell cycle was blocked at S phase of HepG2 cells treated with 9a by flow cytometry detection. Our results provided a basis for the development of a new series of anti-cancer candidates.

A series of cycloberberine derivatives were designed, synthesized and evaluated for their anti-cancer activities in vitro. Among these analogs, compounds 6c, 6e and 6g showed strong inhibition on human HepG2 cells. They afforded a potent effect against DOX-resistant MCF-7 breast cells as well. The primary mechanism showed that cell cycle was blocked at G2/M phase of HepG2 cells treated with 6g using flow cytometry assay. It significantly inhibited the activity of DNA Top I at the concentration of 0.1 mg mL-1. Our results provided a basis for the development of this kind of compounds as novel anti-cancer agents.

The pathological processes of neurodegeneration and neurodegenerative changes after traumatic brain injury (TBI) are closely related to microglia. The pathophysiological functions of microglia are closely correlated to their different cell subtypes. Disease-related microglia (DAM) are a special subtype of microglia, which recently discover on the lesions of degenerative diseases of the central nervous system. DAM are identified as important cells that induce neurodegeneration. The in-depth discussion of DAM role in pathological mechanism of neurodegeneration after TBI provides new clues for understanding and treating neurodegeneration after TBI; therefore, this article focuses on the above content and summarizes the research progress of DAM and neurodegeneration after TBI.

The pathological process continues to evolve for a long time after acute phase of traumatic brain injury (TBI), often coupling with neurodegeneration and neurodegenerative complications. Microvascular dysfunction and blood-brain barrier (BBB) dysfunction caused by neurovascular unit (NVU) dysfunction are closely related to the pathological process of many neurodegenerative diseases. The study on the pathological mechanism of neurovascular unit dysfunction is a promising research field of TBI-related neurodegeneration, and also provides a new idea for the treatment of neurodegeneration after TBI. Therefore, this article mainly reviews these.