Abstract
Cryptotanshinone (CTN), a monomer compound extracted from the dried roots and rhizomes of Salvia miltiorrhiza Bge, has a variety of pharmacological effects. However, little research has been done on the mechanism of CTN in attenuating neuroinflammation. The present study aimed to investigate whether CTN can ameliorate neuroinflammation induced by lipopolysaccharide (LPS) through the Nrf2/heme-oxygenase 1 (HO-1) signaling pathway in BV-2 microglial cells. We found that CTN attenuated the upregulated expression of inducible nitric oxide synthase, cyclooxygenase 2, NOD-like receptor pyrin domains-3, and nitric oxide induced by LPS in microglial cells. In addition, it curtailed the increased release of pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α in LPS-activated microglial cells. Furthermore, CTN significantly increased the levels of NF-κB, Nrf2, HO-1, and Akt proteins. We demonstrated that the anti-inflammatory action of CTN in BV-2 microglial cells was partially through the activation of the Nrf2/HO-1 pathway, which was regulated by the PI3K/Akt signaling pathway. Taken together, our results indicated that CTN downregulated the production and release of proinflammatory mediators in BV-2 microglial cells through activating the Nrf2/HO-1 pathway and subsequently protected neurons from inflammatory injury.
Highlights
Neuroinflammation and oxidative stress play an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer’s Disease (AD) and Parkinson’s disease (PD)
We found that CTN attenuated the upregulated expression of inducible nitric oxide synthase, cyclooxygenase 2, NOD-like receptor pyrin domains-3, and nitric oxide induced by LPS in microglial cells
We demonstrated that the anti-inflammatory action of CTN in BV-2 microglial cells was partially through the activation of the Nrf2/heme-oxygenase 1 (HO-1) pathway, which was regulated by the PI3K/Akt signaling pathway
Summary
Neuroinflammation and oxidative stress play an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer’s Disease (AD) and Parkinson’s disease (PD). Microglial cells, activated by lipopolysaccharide (LPS), are commonly used for in vitro studies on neuroinflammation-related diseases (Velagapudi et al, 2014; Nam et al, 2018). Microglial cells increase the expression of nuclear factor-kappaB (NF-κB) to induce the activity of proinflammatory proteases such as inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2). Proinflammatory mediators such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 were released. Overproduction of these proinflammatory mediators results in neurodegeneration or even
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