Ten phenolic compounds were isolated from a butanol fraction of sage extracts. Their structures were determined by spectral methods (NMR, MS, IR). Among them, a novel compound, 4-hydroxyacetophenone-4-O-β-D-apiofuranosyl-(1f6)-O-β-D-glucopyranoside, was identified. Two test systems, DPPH free radical scavenging activity and radical cation ABTS •+ scavenging activity, were used to evaluate their antioxidant activity. The most active compounds were found to be rosmarinic acid and luteolin-7-O-β-glucopyranoside.

Artichoke leaf is an herbal medicine known for a long time. A systematic antioxidant activity-directed fractionation procedure was used to purify antioxidative components from the aqueous methanol extractions of artichoke heads and leaves in this study. Seven active polyphenolic compounds were purified from artichoke, and structural elucidation of each was achieved using MS and NMR. Two of these compounds, apigenin-7-rutinoside and narirutin, were found to be unique to artichoke heads, this represents the first report of these compounds in the edible portion of this plant. The contents of these antioxidants and total phenols in dried artichoke samples from leaves and immature and mature heads of three varieties, Imperial Star, Green Globe, and Violet, were then analyzed and compared by colorimetric and validated HPLC methods. Significant differences by variety and plant organ were observed.

In Arabidopsis thaliana, a family of six genes (ACBP1 to ACBP6) encodes acyl-CoA binding proteins (ACBPs). Investigations on ACBP3 reported here show its upregulation upon dark treatment and in senescing rosettes. Transgenic Arabidopsis overexpressing ACBP3 (ACBP3-OEs) displayed accelerated leaf senescence, whereas an acbp3 T-DNA insertional mutant and ACBP3 RNA interference transgenic Arabidopsis lines were delayed in dark-induced leaf senescence. Acyl-CoA and lipid profiling revealed that the overexpression of ACBP3 led to an increase in acyl-CoA and phosphatidylethanolamine (PE) levels, whereas ACBP3 downregulation reduced PE content. Moreover, significant losses in phosphatidylcholine (PC) and phosphatidylinositol, and gains in phosphatidic acid (PA), lysophospholipids, and oxylipin-containing galactolipids (arabidopsides) were evident in 3-week-old dark-treated and 6-week-old premature senescing ACBP3-OEs. Such accumulation of PA and arabidopsides (A, B, D, E, and G) resulting from lipid peroxidation in ACBP3-OEs likely promoted leaf senescence. The N-terminal signal sequence/transmembrane domain in ACBP3 was shown to be essential in ACBP3-green fluorescent protein targeting and in promoting senescence. Observations that recombinant ACBP3 binds PC, PE, and unsaturated acyl-CoAs in vitro and that ACBP3 overexpression enhances degradation of the autophagy (ATG)-related protein ATG8 and disrupts autophagosome formation suggest a role for ACBP3 as a phospholipid binding protein involved in the regulation of leaf senescence by modulating membrane phospholipid metabolism and ATG8 stability in Arabidopsis. Accelerated senescence in ACBP3-OEs is dependent on salicylic acid but not jasmonic acid signaling.

Lactobacillus plantarum (L. plantarum) is a well-known probiotic among the ingested-microorganism probiotics (i.e., ingested microorganisms associated with beneficial effects for the host). However, few studies have examined the effects of L. plantarum TWK10 (LP10) supplementation on exercise performance, physical fatigue, and gut microbial profile. Male Institute of Cancer Research (ICR) strain mice were divided into three groups (n = 8 per group) for oral administration of LP10 for six weeks at 0, 2.05 × 108, or 1.03 × 109 colony-forming units/kg/day, designated the vehicle, LP10-1X and LP10-5X groups, respectively. LP10 significantly decreased final body weight and increased relative muscle weight (%). LP10 supplementation dose-dependently increased grip strength (p < 0.0001) and endurance swimming time (p < 0.001) and decreased levels of serum lactate (p < 0.0001), ammonia (p < 0.0001), creatine kinase (p = 0.0118), and glucose (p = 0.0151) after acute exercise challenge. The number of type I fibers (slow muscle) in gastrocnemius muscle significantly increased with LP10 treatment. In addition, serum levels of albumin, blood urea nitrogen, creatinine, and triacylglycerol significantly decreased with LP10 treatment. Long-term supplementation with LP10 may increase muscle mass, enhance energy harvesting, and have health-promotion, performance-improvement, and anti-fatigue effects.

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An activity-directed fractionation and purification process was used to identify the antioxidative components of Polygonum multiflorum Thunb. (PM). Dried root of PM was extracted with 95% ethanol and then separated into water, ethyl acetate, and hexane fractions. Among these only the ethyl acetate phase showed strong antioxidant activity by the 2,2-diphenyl-1-picrylhydrazyl (DPPH) test when compared with water and hexane phases. The ethyl acetate fraction was then subjected to separation and purification using silica gel column chromatography and Sephadex LH-20 chromatography. Three compounds showing strong antioxidant activity were identified by spectral methods ((1)H NMR, (13)C NMR, and MS) and by comparison with authentic samples to be gallic acid, catechin, and 2,3,5, 4'-tetrahydroxystilbene 2-O-beta-D-glucopyranoside.

Cinnamon bark has been reported to be effective in the alleviation of diabetes through its antioxidant and insulin-potentiating activities. In this study, the inhibitory effect of cinnamon bark on the formation of advanced glycation endproducts (AGEs) was investigated in a bovine serum albumin (BSA)-glucose model. Several phenolic compounds, such as catechin, epicatechin, and procyanidin B2, and phenol polymers were identified from the subfractions of aqueous cinnamon extract. These compounds showed significant inhibitory effects on the formation of AGEs. Their antiglycation activities were not only brought about by their antioxidant activities but also related to their trapping abilities of reactive carbonyl species such as methylglyoxal (MGO), an intermediate reactive carbonyl of AGE formation. Preliminary study on the reaction between MGO and procyanidin B2 revealed that MGO-procyanidin B2 adducts are primary products which are supposed to be stereoisomers. This is the first report that proanthocyanidins can effectively scavenge reactive carbonyl species and thus inhibit the formation of AGEs. As proanthocyanidins behave in a similar fashion as aminoguanidine (AG), the first AGE inhibitor explored in clinical trials, they show great potential to be developed as agents to alleviate diabetic complications.

Advanced glycation end-products (AGEs) are the final products of the non-enzymatic reaction between reducing sugars and amino groups in proteins, lipids and nucleic acids. Recently, the accumulation of AGEs in vivo has been implicated as a major pathogenic process in diabetic complications, atherosclerosis, Alzheimer's disease and normal aging. The early recognition of AGEs can ascend to the late 1960s when a non-enzymatic glycation process was found in human body which is similar to the Maillard reaction. To some extent, AGEs can be regarded as products of the Maillard reaction. This review firstly introduces the Maillard reaction, the formation process of AGEs and harmful effects of AGEs to human health. As AGEs can cause undesirable diseases or disorders, it is necessary to investigate AGE inhibitors to offer a potential therapeutic approach for the prevention of diabetic or other pathogenic complications induced by AGEs. Typical effective AGE inhibitors with different inhibition mechanisms are also reviewed in this paper. Both synthetic compounds and natural products have been evaluated as inhibitors against the formation of AGEs. However, considering toxic or side effects of synthetic molecules present in clinical trials, natural products are more promising to be developed as potent AGE inhibitors.