Alcoholic liver disease (ALD) is a mounting public health problem with significant medical, economic and social burdens. Tartary buckwheat (F. tataricum (L.) Gaertn, bitter buckwheat) is a kind of healthy and nutritious food, which has been demonstrated to protect against ALD, but the underlying mechanism has not been fully studied. Herein, we aimed to elucidate the beneficial effects of Tartary buckwheat extract (mainly composed of polyphenols including rutin, quercetin, kaempferol and kaempferol-3-O-rutinoside) in terms of lipid metabolism with the aid of lipidomic analysis. In our study, we employed C57BL/6J mice and a Lieber–DeCarli alcohol liquid diet to construct an ALD model and found that Tartary buckwheat extract was able to prevent ALD-induced histopathological lesions, liver injury and abnormal plasma lipid levels. These beneficial effects might be attributed to the regulation of energy metabolism-related genes (SIRT1, LKB1 and AMPK), lipid synthesis-related genes (ACC, SREBP1c and HMGR) and lipid oxidation-related genes (PPARα, CPT1 and CPT2). In addition, lipidomic profiling and KEGG pathway analysis showed that glycerophospholipid metabolism contributed the most to elucidating the regulatory mechanism of Tartary buckwheat extract. In specific, chronic ethanol intake reduced the level of phosphatidylcholines (PC) and increased the level of phosphatidylethanolamines (PE) in the liver, resulting in a decrease in the PC/PE ratio, which could be all significantly restored by Tartary buckwheat extract intervention, indicating that the Tartary buckwheat extract might regulate PC/PE homeostasis to exert its lipid-lowering effect. Overall, we demonstrated that Tartary buckwheat extract could prevent ALD by modulating hepatic glycerophospholipid metabolism, providing the theoretical basis for its further exploitation as a medical plant or nutritional food.

Juices, wine, coffee, and cocoa are rich sources of natural polyphenolic compounds that have potent antioxidant activities proven by in vitro and in vivo studies. These polyphenolic compounds quench reactive oxygen and nitrogen species (RONS) or reactive free radicals and act as natural antioxidants which are also able to protect against reactive oxygen species (ROS)-mediated oxidative damage, which elevates cellular antioxidant capacity to induce antioxidant defense mechanisms by modulating transcription factors. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a transcription factor encoded in humans. It is activated as a result of oxidative stress and induces the expression of its target genes. This is one of the most important cellular defense mechanisms against oxidative stress. However, the oxidative stress alone is not enough to activate Nrf2. Hence phytochemicals, especially polyphenolics, act as natural Nrf2 activators. Herein, this review discusses the natural products identified in juices, coffee, cocoa and wines that modulate Nrf2 activity in cellular systems.

Astragalus membranaceus is a famous herb found among medicinal and food plants in East and Southeastern Asia. The Nrf2-ARE assay-guided separation of an extract from Jing liqueur led to the identification of a nontoxic Nrf2 activator, methylnissolin-3-O-β-d-glucopyranoside (MNG, a component of A. membranaceus). Nrf2 activation by MNG has not been reported before. Using Western Blot, RT-qPCR and imaging, we investigated the cytoprotective effect of MNG against hydrogen peroxide-induced oxidative stress. MNG induced the expression of Nrf2, HO-1 and NQO1, accelerated the translocation of Nrf2 into nuclei, and enhanced the phosphorylation of AKT. The MNG-induced expression of Nrf2, HO-1, and NQO1 were abolished by Nrf2 siRNA, while the MNG-induced expression of Nrf2 and HO-1 was abated and the AKT phosphorylation was blocked by LY294002 (a PI3K inhibitor). MNG reduced intracellular ROS generation. However, the protection of MNG against the H₂O₂ insult was reversed by Nrf2 siRNA with decreased cell viability. The enhancement of Nrf2 and HO-1 by MNG upon H₂O₂ injury was reduced by LY294002. These data showed that MNG protected EA.hy926 cells against oxidative damage through the Nrf2/HO-1 and at least partially the PI3K/Akt pathways.

Background and Objective. Qingke (Tibetan hulless barley, Hordeum vulgare L.) contains a high content of β-glucan among all the cereal varieties. Although β-glucan has multiple physiological functions, the physiological function of qingke β-glucan was few studied. In this study, the β-glucan was isolated, purified, determined the structural characterization, and measured the inhibitory activity to enzymes correlating blood sugar and lipid. Methods. β-Glucan was isolated from enzymatic aqueous extract of qingke by using deproteinization, decolorization, DEAE-52 column chromatography, and sepharose CL-4B agarose gel column chromatography. The structure of the β-glucan was determined using FT-IR and ¹³C-NMR spectra analysis, and molecular mass by use of HPSEC-dRI-LS. The kinematic viscosity was measured. The inhibitory effects of this β-glucan on four enzymes were investigated. Results. This β-glucan had a uniform molecular weight of 201,000 Da with β-(1⟶4) as the main chain and β-(1⟶3) as a side chain. The β-glucan presented a relatively strong inhibitory activity on α-glucosidase, moderate inhibition on invertase, and a weak inhibition on α-amylase, whereas it did not inhibit lipase. Conclusion. The study indicates that the enzymatic β-glucan from qingke has the potential as natural auxiliary hypoglycemic additives in functional medicine or foods.

As a traditional Chinese medicinal herb, ginseng (Panax ginseng C. A. Mey.) is commonly used to treat common diseases, for example, esophageal cancer and myasthenia gravis. Furthermore, ginseng is also processed into a functional food additive that is utilized to improve the freshness of chicken soup and make health wine. Unfortunately, ginseng (Panax ginseng C. A. Mey.) has already shown a noticeable bitterness during its application process. In this research, the bitter substances in ginseng (Panax ginseng C. A. Mey.) after two common preparation processes (water extraction and ethanol extraction) were separated, purified and identified by preparative high performance liquid chromatography (prep-HPLC), high performance liquid chromatography with diode array detector (HPLC-DAD), ultra-performance liquid chromatography coupled with high-resolution quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) and an electronic tongue. The results indicated that compared with the other four bitter compounds, the ginsenoside Rb1 had the highest bitterness value, followed by 20(S)-ginsenoside Rg2, ginsenoside Rg1, ginsenoside Rf and ginsenoside Rb3. Upon the evaluation of results to reduce the bitterness of ginseng extract, we found that the composite embedding system of chitosan adsorption in the ginseng carrageenan gel microsphere (K/M_C/M_CG) could effectively reduce the bitterness.

Background: As known, inhibition of phosphodiesterase 5 (PDE5) has the therapeutic effect on male erectile dysfunction (ED), and the processed folium of Epimedium sagittatum Maxim. (PFES) characterized by 8-isopentenyl flavonoids is a famous herb for treating ED. However, the main flavonoids inhibitory activities, structure–activity relationship (SAR) and signaling pathway have been not systematically studied so that its pharmacodynamic mechanism is unclear. Methods: We aimed to initially reveal the PFES efficacy mechanism for treating ED. For the first time, 6 main 8-isopentenyl flavonoids (1–6) from PFES were isolated and identified. Then based on HPLC detection, we proposed a novel method to screen inhibitors among them. We further analyze the three-dimensional quantitative structure–activity relationship (3D-QSAR) for those inhibitors. Results: The results were verified by cellular effects of the screened flavonoids. Among 6 compounds, Icariin: (1), 2-Oʹʹrhamnosylicaridide II (2) and Baohuoside I (3) were identified with significant activities (IC₅₀ = 8.275, 3.233, 5.473 μM). Then 3D-QSAR studies showed that the replacement of C8 with bulky steric groups as isopentenyl, C3 with positive charge groups and C4' with a hydrogen bond acceptor substituent could increase inhibitory effects. In contrast, the substitution of C7 with bulky steric groups or hydrophilic groups tended to decrease the efficacies. And compounds 1, 2, 3 could increase cGMP level and decrease cytoplasmic Ca²⁺ of rat corpus cavernosum smooth muscle cells (CCSMCs)by activating PKG. Conclusion: 8-isopentenyl flavonoids could be the main pharmacodynamic substances of PFES in the treatment for ED, and some had significant PDE5A1 inhibitory activities so as to activate cGMP/PKG/Ca²⁺ signaling pathway in CCSMCs, that was related to the substituents at the key sites such as C8, C3, C4ʹ and C7 in the characteristic compounds.