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. 2019 Oct 13;20(20):5081.
doi: 10.3390/ijms20205081.

Green Tea Polyphenol (-)-Epigallocatechin Gallate (EGCG) Attenuates Neuroinflammation in Palmitic Acid-Stimulated BV-2 Microglia and High-Fat Diet-Induced Obese Mice

Limin Mao  1 , Danielle Hochstetter  2 , Liyun Yao  3 , Yueling Zhao  4 , Jihong Zhou  5 , Yuefei Wang  6 , Ping Xu  7
Affiliations

Green Tea Polyphenol (-)-Epigallocatechin Gallate (EGCG) Attenuates Neuroinflammation in Palmitic Acid-Stimulated BV-2 Microglia and High-Fat Diet-Induced Obese Mice

Limin Mao et al. Int J Mol Sci. .

Abstract

Obesity is closely associated with neuroinflammation in the hypothalamus, which is characterized by over-activated microglia and excessive production of pro-inflammatory cytokines. The present study was aimed at elucidating the effects of (-)-epigallocatechin gallate (EGCG) on palmitic acid-stimulated BV-2 microglia and high-fat-diet-induced obese mice. The results indicated the suppressive effect of EGCG on lipid accumulation, pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) release, and microglial activation in both cellular and high-fat-diet rodent models. These results were associated with lower phosphorylated levels of the janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) signaling pathway. In conclusion, EGCG can attenuate high-fat-induced hypothalamic inflammation via inhibiting the JAK2/STAT3 signaling pathways in microglia.

Keywords: hypothalamus; inflammation; obesity; saturated fatty acids; tea polyphenols.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Effects of (−)-epigallocatechin gallate (EGCG) on lipid accumulation and inflammatory responses of PA-stimulated BV-2 cells. BV2 cells were pretreated with different dosages of EGCG (EL: low concentration of EGCG (5 μM), EM: medium concentration of EGCG (10 μM), EH: high concentration of EGCG (20 μM)) for 2 h and then stimulated with 200 μM palmitic acid (PA) for 24 h. (a) Lipid distribution in BV-2 cells was observed by oil red O staining and analyzed with ImageJ; lipids were stained red; (b) Levels of TNF-α, IL-6, and IL-1β in the conditioned medium were measured by ELISA. Data are means ± SEM of three independent experiments performed in triplicate. Different superscript letters indicate significantly different means at p < 0.05 (a > b > c > d).
Figure 1
Figure 1
Effects of (−)-epigallocatechin gallate (EGCG) on lipid accumulation and inflammatory responses of PA-stimulated BV-2 cells. BV2 cells were pretreated with different dosages of EGCG (EL: low concentration of EGCG (5 μM), EM: medium concentration of EGCG (10 μM), EH: high concentration of EGCG (20 μM)) for 2 h and then stimulated with 200 μM palmitic acid (PA) for 24 h. (a) Lipid distribution in BV-2 cells was observed by oil red O staining and analyzed with ImageJ; lipids were stained red; (b) Levels of TNF-α, IL-6, and IL-1β in the conditioned medium were measured by ELISA. Data are means ± SEM of three independent experiments performed in triplicate. Different superscript letters indicate significantly different means at p < 0.05 (a > b > c > d).
Figure 2
Figure 2
Inhibition effect of (−)-epigallocatechin gallate (EGCG) on JAK2/STAT3 signaling activation in PA-stimulated BV-2 cells. BV-2 cells were pretreated with 20 μM EGCG for 2 h and then stimulated with 200 μM palmitic acid for 24 h. Representative Western blots for JAK2 and STAT3 phosphorylation in BV-2 cells were shown. Data are means ± SEM of three independent experiments performed in triplicate. Different superscript letters indicate significantly different means at p < 0.05 (a > b > c).
Figure 3
Figure 3
Effect of (−)-epigallocatechin gallate (EGCG) on HFD-induced obesity. (a) Weight variation tendency of different groups; (b) Weight of epididymis adipose; (c) Representative hematoxylin and eosin (H&E) staining of epididymis adipose sections. Data are means ± SEM (n = 6). Different superscript letters indicate significantly different means at p < 0.05 (a > b > c).
Figure 4
Figure 4
Inhibition effect of (−)-epigallocatechin gallate (EGCG) on obesity-associated neuroinflammation of hypothalamus. (a) Concentrations of TNF-α, IL-6, IL-1β in the hypothalamus; (b) Representative Western blots for JAK2 and STAT3 phosphorylation levels in the hypothalamus; (c) Representative micrographs of immunofluorescence labeling for Iba1 in the hypothalamic arcuate nucleus (ARC) and paraventricular nucleus (PVN) (outlined by white dashed lines) and higher magnification insets (outlined by white solid lines). Data are means ± SEM of three independent experiments performed in triplicate (n = 3). Different superscript letters indicate significantly different means at p < 0.05 (a > b > c).
Figure 5
Figure 5
Possible neurological mechanisms of (−)-epigallocatechin gallate (EGCG) on HFD-induce obesity.
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