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. 2017 Feb 2;197:92-100.
doi: 10.1016/j.jep.2016.07.073. Epub 2016 Jul 26.

The Ayurvedic Plant Bacopa Monnieri Inhibits Inflammatory Pathways in the Brain

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The Ayurvedic Plant Bacopa Monnieri Inhibits Inflammatory Pathways in the Brain

Michelle D Nemetchek et al. J Ethnopharmacol. .
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Abstract

Ethnopharmacological relevance: Bacopa monnieri (L) Wettst (common name, bacopa) is a medicinal plant used in Ayurveda, the traditional system of medicine of India, as a nootropic. It is considered to be a "medhya rasayana", an herb that sharpens the mind and the intellect. Bacopa is an important ingredient in many Ayurvedic herbal formulations designed to treat conditions such as memory loss, anxiety, poor cognition and loss of concentration. It has also been used in Ayurveda to treat inflammatory conditions such as arthritis. In modern biomedical studies, bacopa has been shown in animal models to inhibit the release of the pro-inflammatory cytokines TNF-α and IL-6. However, less is known regarding the anti-inflammatory activity of Bacopa in the brain.

Aim of the study: The current study examines the ability of Bacopa to inhibit the release of pro-inflammatory cytokines from microglial cells, the immune cells of the brain that participate in inflammation in the CNS. The effect of Bacopa on signaling enzymes associated with CNS inflammatory pathways was also studied.

Materials and methods: Various extracts of Bacopa were prepared and examined in the N9 microglial cell line in order to determine if they inhibited the release of the proinflammatory cytokines TNF-α and IL-6. Extracts were also tested in cell free assays as inhibitors of caspase-1 and matrix metalloproteinase-3 (enzymes associated with inflammation) and caspase-3, which has been shown to cleave protein Tau, an early event in the development of Alzheimer's disease.

Results: The tea, infusion, and alkaloid extracts of bacopa, as well as Bacoside A significantly inhibited the release of TNF-α and IL-6 from activated N9 microglial cells in vitro. In addition, the tea, infusion, and alkaloid extracts of Bacopa effectively inhibited caspase 1 and 3, and matrix metalloproteinase-3 in the cell free assay.

Conclusions: Bacopa inhibits the release of inflammatory cytokines from microglial cells and inhibits enzymes associated with inflammation in the brain. Thus, Bacopa can limit inflammation in the CNS, and offers a promising source of novel therapeutics for the treatment of many CNS disorders.

Keywords: 1.04 Central nervous system; 2.104-Anxiolytic; 2.132—Ayurveda; 2.348—Inflammation; 2.476—phytochemistry; 2.548—signal transduction; Bacopa; Caspases; Cytokines; Inflammation; Microglia.

Figures

Figure 1
Figure 1
MTS assay of concentrations of bacopa extracts (μg/ml) in N9 microglial cell cultures following 24h of treatment. None of the concentrations of the infusion (A), tea (B), or alkaloid (C) fraction resulted in cell death. The double asterisks indicate that cell death occurred at 6 μg/ml of the Bacoside A (D). There were small but significant increases in cell survival compared to media controls in the 12.5 μg/ml tea, the 0.125 and 025 μg/ml alkaloid, and the 1.5 μg/ml Bacoside A suggesting that these concentrations are beneficial for cell survival. Graphs represent mean ± SEM. *p<0.05; ANOVA with Dunnett's post hoc test compared to media control.
Figure 2
Figure 2
IL-6 release from non-activated N9 microglial cells following a 24 h incubation with the bacopa extracts. The infusion (A) and tea (B) extracts induce a very small but significant release in IL-6 at the two highest concentrations of the extracts. Neither the alkaloid fraction (C) nor the Bacoside A (D) results in increased release of IL-6 compared to media controls. Graphs represent mean ± SEM. *p<0.05; ANOVA with Dunnett's post hoc test compared to media control.
Figure 3
Figure 3
TNF-α release from non-activated N9 microglial cells following a 24 h incubation with the bacopa extracts. Neither the infusion (A), or alkaloid (C) fractions or the Bacoside A (D) induces an increase in the release of TNF-α from the microglial cells compared to media controls. The highest concentration of the tea extract (B) results in a small but significant release of TNF-α compared to the media control. Graphs represent mean ± SEM. *p<0.05; ANOVA with Dunnett's post hoc test compared to media control.
Figure 4
Figure 4
IL-6 release from LPS-activated N9 microglial following a 24 h incubation with LPS plus the bacopa extracts. The infusion extract significantly inhibited the release of IL-6 from Fi LPS activated microglial at 25 and 50 μg compared to LPS controls (A). The highest concentration of the alkaloid fraction (1 μg) also inhibited the release of IL-6 from activated microglia (C). Neither the tea nor the Bacoside A significantly inhibited IL-6 release compared to LPS controls (B and D). Data is normalized to IL-6 release from LPS activation only. Graphs represent mean ± SEM. *p<0.05; ANOVA with Dunnett's post hoc test compared to LPS control.
Figure 5
Figure 5
TNF-α release from LPS activated N9 microglial cells following a 24 h incubation with bacopa plus the extracts. Both the infusion (A) and the alkaloid (C) fraction showed significant inhibition of the release of TNF-α from LPS activated microglia of approximately 20%-27% compared to LPS alone. The tea extract (B) did not inhibit the release of TNF-α. The Bacoside A (D) showed a small but significant increase in TNF-α release at the highest concentration. Data is normalized to TNF-α release from LPS activation only. Graphs represent mean ± SEM. *p<0.05; ANOVA with Dunnett's post hoc test compared to LPS control.
Figure 6
Figure 6
Each bacopa extract was evaluated for its ability to inhibit caspase-1, caspase-3, and MMP-3 in 96 well assays. These data are expressed in terms of % inhibition of enzyme activity. Control 1 included the substrate and enzyme (no inhibitor) and Control 2 included the substrate, enzyme and a specific inhibitor (as described).

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