State Key Laboratory of Tea Plant Biology and Utilization, School of Tea and Food Science & Technology , Anhui Agricultural University , Hefei , Anhui 230036 , China.
International Joint Laboratory on Tea Chemistry and Health Effects , Anhui Agricultural University , Hefei , Anhui 230036 , China.
J Agric Food Chem. 2018 Jul 25;66(29):7674-7683. doi: 10.1021/acs.jafc.8b02293. Epub 2018 Jul 12.
Theanine, a unique bioactive constituent from tea ( Camellia sinensis) leaves, is widely used as a functional ingredient and dietary supplement. To evaluate the anti-inflammatory and hepatoprotective effects of theanine and its molecular mechanism, the lipopolysaccharide (LPS)-induced inflammation mouse model was employed in this study. The survival rate of mice in the theanine-treated group increased significantly compared with that of LPS-only group mice. Furthermore, ICR male mice were randomly divided into three or four groups: control, LPS (LPS treatment only), LPS + theanine (20 mg/kg/day), and theanine (theanine treatment only). The results showed that compared with the LPS group, the liver damage and oxidative stress of the theanine-treated group decreased significantly, based on plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) concentrations, hepatic total superoxide dismutase (T-SOD), and malondialdehyde (MDA) levels, and histological scores and apoptosis [terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) staining and caspase-3 activity] in the liver tissues. Furthermore, compared with no treatment, pretreatment with theanine significantly decreased the release of interleukin (IL)-1β and tumor necrosis factor (TNF)-α, inhibited the expression of several inflammatory factors (including IL-1β, TNF-α, and IL-6), and increased the IL-10/interferon (IFN)-γ ratio in the hepatic tissues. In the LPS-induced inflammation model, theanine inhibited the expression of proinflammatory mediators involved in the nuclear factor-kappa B (NF-κB) pathway, such as inducible nitric oxide synthase (iNOS) and matrix metalloproteinase-3 (MMP-3), and attenuated the phosphorylation of NF-κB in the hepatic tissues. Moreover, theanine suppressed the acute-phase response (elevated nitric oxide and C-reactive protein levels). Furthermore, theanine suppressed the LPS-induced inflammatory state by normalizing hypothalamic-pituitary-adrenal (HPA) axis hyperactivity. Taken together, the results suggest that theanine potentially ameliorates LPS-induced inflammation and acute liver injury; molecular mechanism of action may involve normalization of HPA axis hyperactivity and inactivation of the NF-κB signaling pathway.
茶氨酸是茶叶中的一种独特的生物活性成分，被广泛用作功能成分和膳食补充剂。为了评估茶氨酸的抗炎和保肝作用及其分子机制，本研究采用脂多糖（LPS）诱导的炎症小鼠模型。与 LPS 组相比，茶氨酸治疗组小鼠的存活率显著提高。此外，将 ICR 雄性小鼠随机分为三组或四组：对照组、LPS（仅 LPS 处理）、LPS+茶氨酸（20mg/kg/天）和茶氨酸（仅茶氨酸处理）。结果表明，与 LPS 组相比，茶氨酸治疗组的肝损伤和氧化应激明显减轻，基于血浆丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）浓度、肝总超氧化物歧化酶（T-SOD）和丙二醛（MDA）水平以及组织学评分和肝组织中的细胞凋亡[末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸缺口末端标记（TUNEL）染色和半胱天冬酶-3 活性]。此外，与未处理相比，茶氨酸预处理显著降低白细胞介素（IL）-1β和肿瘤坏死因子（TNF）-α的释放，抑制几种炎症因子（包括 IL-1β、TNF-α和 IL-6）的表达，并增加肝组织中的 IL-10/干扰素（IFN）-γ比值。在 LPS 诱导的炎症模型中，茶氨酸抑制核因子-κB（NF-κB）途径中参与的促炎介质的表达，如诱导型一氧化氮合酶（iNOS）和基质金属蛋白酶-3（MMP-3），并减弱肝组织中 NF-κB 的磷酸化。此外，茶氨酸抑制急性期反应（升高的一氧化氮和 C 反应蛋白水平）。此外，茶氨酸通过调节下丘脑-垂体-肾上腺（HPA）轴的过度活跃来抑制 LPS 诱导的炎症状态。总之，结果表明茶氨酸可能改善 LPS 诱导的炎症和急性肝损伤；作用的分子机制可能涉及调节 HPA 轴的过度活跃和抑制 NF-κB 信号通路。
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