Chronic inflammation in the brain plays a critical role in major neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Microglia, the resident macrophages and intrinsic components of the central nervous system (CNS), appear to be the main effectors in this pathological process. Magnesium lithospermate B (MLB) is one of the major bioactive components of Radix Salviae miltiorrhizae, which has been documented to protect neurons against multiple types of neuronal injury. However, its functions on microglia and the related neuroinflammation remain unknown. In the present study, BV2 microglial cells were used to assess the anti-neuroinflammatory capacity of MLB. Our data show that treatment with MLB could not only suppress lipopolysaccharide (LPS)-induced proliferation and morphological changes, but also interfere with cell cycle progression in BV2 cells. More strikingly, it attenuated the production of the inflammatory mediator nitric oxide (NO) and a panel of pro-inflammatory cytokine in LPS-stimulated BV2 cells, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1α, IL-1β, and IL-6, and also promoted a phenotypic switch from the M1 to the M2 phenotype. Additionally, an in vivo study showed that the administration of MLB could ameliorate lipopolysaccharide-induced neurodegeneration and microglial activation in the hippocampus of adult mice. Mechanistically, MLB blocked the activation of the NF-κB pathway upon LPS stimulation, indicating that the effects of MLB on microglia may be mediated by the NK-κB pathway. These results suggest the therapeutic potential of MLB as a novel anti-inflammatory and microglia-modulating drug for neurodegenerative diseases.

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Colorectal cancer (CRC) is a common malignant tumor of the digestive system worldwide. DMC-BH, a curcumin analog, has been reported to possess anticancer properties against human gliomas. However, its effects and mechanism on CRC cells are still unknown. Our present study demonstrated that DMC-BH had stronger cytostatic ability than curcumin against CRC cells in vitro and in vivo . It effectively inhibited the proliferation and invasion and promoted the apoptosis of HCT116 and HT-29 cells. RNA-Seq and data analysis indicated that its effects might be mediated by regulation of the PI3K/AKT signaling. Western blotting further confirmed that it dose-dependently suppressed the phosphorylation of PI3K, AKT and mTOR. The Akt pathway activator SC79 reversed the proapoptotic effects of DMC-BH on CRC cells, indicating that its effects are mediated by PI3K/AKT/mTOR signaling. Collectively, the results of the present study suggest that DMC-BH exerts more potent effects than curcumin against CRC by inactivating the PI3K/AKT/mTOR signaling pathway.