Kinkéliba (Combretum micranthum) Leaf Extract Alleviates Skin Inflammation: In Vitro and In Vivo Study.

Kinkéliba (Combretum micranthum, Seh-Haw in Wolof) is a popular bush tea in West African countries. Although the kinkéliba plant's leaves have been widely consumed for its nutritional and medicinal properties, its benefits on skin health potential have been practically untouched. In human epidermal primary keratinocytes, vitexin and isovitexin-rich kinkéliba extract treatment significantly (p < 0.001) enhanced up to 39.6% of the cell survival rate decreased by UV radiation irritation. The treatment of kinkéliba leaf extracts also reduced the production of UV-induced pro-inflammatory cytokines IL-6 and IL-8 by 57.6% and 42.5%, respectively (p < 0.001), which cause skin redness and skin barrier dysfunction, as well as wrinkles and collagen degradation. The anti-inflammation efficacy of kinkéliba leaf extracts might involve significant inhibition on the levels of cellular reactive oxygen species (ROS) (-70.8%, p < 0.001) and nitrotyrosine (-56.9%, p < 0.05). Further topical applications of kinkéliba leaf extract gel were found to reduce sodium lauryl sulfate (SLS)-induced skin inflammation: at D7, the skin trans-epidermal water loss (TEWL) and skin redness (a* value) were both reduced by 59.81% (p < 0.001) and 22.4% (p < 0.001), compared with D0. In vitro and in vivo data support a new topical application of the kinkéliba leaf as an effective active ingredient for the treatment of skin inflammation, as well as subsequent barrier dysfunction and inflammaging.

The transcription factor StTINY3 enhances cold-induced sweetening resistance by coordinating starch resynthesis and sucrose hydrolysis in potato.

The accumulation of reducing sugars in cold-stored tubers, known as cold-induced sweetening (CIS), negatively affects potato processing quality. The starch to sugar interconversion pathways that are altered in cold-stored CIS tubers have been elucidated, but the mechanism that regulates them remains largely unknown. This study identified a CBF/DREB transcription factor (StTINY3) that enhances CIS resistance by both activating starch biosynthesis and repressing the hydrolysis of sucrose to reducing sugars in detached cold-stored tubers. Silencing StTINY3 in a CIS-resistant genotype decreased CIS resistance, while overexpressing StTINY3 in a CIS-sensitive genotype increased CIS resistance, and altering StTINY3 expression was associated with expression changes in starch resynthesis-related genes. We showed first that overexpressing StTINY3 inhibited sucrose hydrolysis by enhancing expression of the invertase inhibitor gene StInvInh2, and second that StTINY3 promoted starch resynthesis by up-regulating a large subunit of the ADP-glucose pyrophosphorylase gene StAGPaseL3, and the glucose-6-phosphate transporter gene StG6PT2. Using electrophoretic mobility shift assays, we revealed that StTINY3 is a nuclear-localized transcriptional activator that directly binds to the dehydration-responsive element/CRT cis-element in the promoters of StInvInh2 and StAGPaseL3. Taken together, these findings established that StTINY3 influences CIS resistance in cold-stored tubers by coordinately modulating the starch to sugar interconversion pathways and is a good target for improving potato processing quality.

The depigmenting effect of natural resorcinol type polyphenols Kuwanon O and Sanggenon T from the roots of morus australis.

ETHNOPHARMACOLOGICAL RELEVANCE: Morus australis, one of the major Morus species growing in East Asia, is rich in phenolic compounds. The extract of M. australis has been used as skin whitening components for a long period. The action mechanisms of its principal constituents are still unclear. This study aims to evaluate the skin lightening effects of phenolic compounds extracted from the root of M. australis in different melanocyte systems and artificial skin models. MATERIALS AND METHODS: The depigmenting effect of resorcinol type polyphenols (RTPs) from the root extract of M. australis was evaluated in murine b16 and melan-a cell lines using a combined sulforhodamine B assay. Tyrosinase activity and the expression of melanogenesis proteins were evaluated for the mechanism study. The artificial skin model is used as a replacement of the animal test. RESULTS: Only Kuwanon O and Sanggenon T were found to have significant depigmenting effects in both murine b16 and melan-a cell lines. Their depigmenting mechanisms are slightly different in the two cell systems. In b16 cells, Kuwanon O and Sanggenon T, together with the other two RTPs, induced post-transcriptional degradations of MITF without suppressing its mRNA expression, leading to significant decreases of TRP-1 and TRP-2 production. While in melan-a cells, the levels of tyrosinase families were suppressed via MITF downregulation at both transcription and translation level by RTPs, with Kuwanon O inducing the greatest suppression. Further evaluations in artificial skin model demonstrated the outstanding depigmenting effects of Kuwanon O and Sanggenon T. CONCLUSIONS: Kuwanon O and Sanggenon T from M.australis root extract are two potential skin whitening ingredients. To screen resorcinol flavonone derivatives with an isoprenyl group in the Diels-Alder substituent might be an option for the search of potent hypopigmenting agents from plants.

Photoprotective effects of oxyresveratrol and Kuwanon O on DNA damage induced by UVA in human epidermal keratinocytes.

Ultraviolet A not only plays a major part in photoaging and skin tanning but also induces genetic damage and mutation in the epidermal basal layer of human skin. The photoprotective effect of oxyresveratrol and kuwanon O, two phenolic compounds from the root extract of Morus australis, in human primary epidermal keratinocytes was investigated in this study. Both of them were nontoxic to cells at a concentration less than 10 and 0.5 µM, respectively. After pretreatment at the concentrations of 5 and 10 µM, oxyresveratrol increased cell viability, exhibited significant suppressions on UVA- or H2O2-induced cellular ROS. UVA-enhanced nitrotyrosine was also reduced by post-treatment with oxyresveratrol at theses concentrations. Kuwanon O presented similar inhibitions on cellular ROS and nitrotyrosine with lower concentrations (0.25 and 0.5 µM), but there is no significant protection on cell survival after UVA irradiation. Their photoprotective effects also involved the enhanced repair of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and cyclobutane pyrimidine dimers (CPDs) as mediated by the augment of p53 expression after UVA radiation.

Effects of Lycium barbarum polysaccharides on oxidative stress in hyperlipidemic mice following chronic composite psychological stress intervention.

Chronic composite psychological stress intervention is the accumulation of factors which may induce psychological stress, including food deprivation, water deprivation and swimming in cold water. Approximately 40% of cases of atherosclerosis are associated with chronic composite psychological stress. The aim of the present study was to explore the effects of Lycium barbarum polysaccharides (LBP) on blood lipid levels and oxidative stress in hyperlipidemic mice, following chronic composite psychological stress. A hyperlipidemic mouse model was generated, and the mice were subjected to chronic composite psychological stress and treated with LBP for 30 days. After 30 days the triglyceride (TG) and total cholesterol (TC) levels were measured in the serum, and the mRNA expression levels of cholesterol 7α­hydroxylase (CYP7A1) were determined in the liver, in order to observe any changes to lipid metabolism. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured in the liver to evaluate the effects of LBP on oxidative stress. The blood serum levels of interleukin­6 (IL­6) and heat shock protein 70 (HSP­70) were measured to evaluate the extent of the aortic inflammatory response, and to determine the protective effects of LBP. The levels of TG, TC, MDA and IL­6 were significantly higher in the mice subjected to chronic composite psychological stress (HS), as compared with the mice treated with LBP alone (HL), or treated with LBP and subjected to stress (HLS). In addition, SOD and HSP­70 levels, and the mRNA expression levels of CYP7A1 were significantly lower in the HS group, as compared with that in the HL and HLS groups. These results suggest that chronic composite psychological stress may promote the occurrence and development of atherosclerosis, by inducing the aortic inflammatory response and lipid peroxidation. Furthermore, treatment with LBP significantly inhibited oxidative stress and the aortic inflammatory response.

Protective effect of oxymatrine on chronic rat heart failure.

Oxymatrine is one of the alkaloids extracted from the Chinese herb Sophora japonica (Sophora flavescens Ait.) with anti-inflammatory, immune reaction inhibiting, antiviral, and hepatocyte and antihepatic fibrosis protective activities. However, the effect of oxymatrine on heart failure is not yet known. In this study, the effect of oxymatrine on heart failure was investigated using a Sprague-Dawley rat model of chronic heart failure. Morphological findings showed that in the group treated with 50 and 100 mg/kg of oxymatrine; intermyofibrillar lysis disappeared, myofilaments were orderly, closely and evenly arranged; and mitochondria contained tightly packed cristae compared with the heart failure group. We investigated the cytosolic Ca(2+) transients and sarcoplasmic reticulum (SR) Ca(2+) content, and assessed the expression of ryanodine receptor (RyR2), SR-Ca(2+) ATPase (SERCA2a), and L-type Ca(2+) channel (dihydropyridine receptor, DHPR). We found that the cytosolic Ca(2+) transients were markedly increased in amplitude in the medium- (ΔF/F (0) = 26.22 ± 2.01) and high-dose groups (ΔF/F (0) = 29.49 ± 1.17) compared to the heart failure group (ΔF/F (0) = 12.12 ± 1.35, P < 0.01), with changes paralleled by a significant increase in the SR Ca(2+) content (medium-dose group: ΔF/F (0) = 32.20 ± 1.67, high-dose group: ΔF/F (0) = 32.57 ± 1.29, HF: ΔF/F (0) = 17.26 ± 1.05, P < 0.01). Moreover, we demonstrated that the expression of SERCA2a and cardiac DHPR was significantly increased in the medium- and high-dose group compared with the heart failure rats. These findings suggest that oxymatrine could improve heart failure by improving the cardiac function and that this amelioration is associated with upregulation of SERCA2a and DHPR.