Anti-Wrinkling and Anti-Melanogenic Effect of Pradosia mutisii Methanol Extract.

Ultraviolet (UV) exposure causes skin photoaging leading to skin wrinkling and sagging via production of reactive oxygen species (ROS). For this reason, protection from photoaging is an important feature in cosmeceutical and dermatological products. Natural product-derived biomaterials are highly desired as future possible ingredients, because these biomaterials are often safe and effective. In this study, we aimed to characterize the skin protective activity of Pradosia mutisii, traditionally used to treat sunburn and erythema. We determined the free radical scavenging, anti-melanogenic, and moisturizing effects of a methanol extract of Pradosia mutisii (Pm-ME) in keratinocytes (HaCaT cells), melanocytes (B16F10 cells), and fibroblasts (human dermal fibroblasts (HDFs)) at non-cytotoxic concentrations. Pradosia mutisii methanol extract contains coumaric acid as a major component, and the extract exhibited protective activity against UVB- and H2O2-induced cytotoxicity. This extract also suppressed the expression of metalloproteinases (MMPs) and cyclooxygenase (COX)-2 in HaCaT cells. A reduction of Sirt-1 expression under UVB- and H2O2-treated conditions was recovered in HaCaT cells by Pm-ME. This extract displayed significant free radical scavenging activity according to the 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulphonic acid) diammonium salt (ABTS) assay. The Pm-ME also upregulated the expression levels of hyaluronic acid synthase (HAS) and transglutaminase-1 (TGM-1) in HaCaT cells, indicating a putative moisturizing activity. Interestingly, the expression of collagen type 1 (Col1A1) gene and its promoter activity, as assessed by a reporter gene assay, were found to be increased in HDF and HEK293 cells. Similarly, Pm-ME helped recover collagen levels after UVB and H2O2 treatment in HDFs as well as decreased the synthesis and secretion of melanin from B16F10 melanoma cells, which may indicate a beneficial whitening cosmetic value. The p38 inhibitor SB203580 and the JNK inhibitor SP600125 suppressed MMP-9 and COX-2 expression in H2O2-treated HaCaT cells. Similarly, the ERK inhibitor U0126 inhibited HAS-2 in Pm-ME/H2O2-treated HaCaT cells. These findings suggested that inhibition of JNK and p38 and activation of ERK could be targeted by Pm-ME. Therefore, Pm-ME may exert anti-photoaging and anti-melanogenic properties via the regulation of mitogen-activated protein kinase, which could be beneficial in the cosmeceutical industry.

Loliolide Presents Antiapoptosis and Antiscratching Effects in Human Keratinocytes.

Loliolide is a monoterpenoid hydroxylactone present in freshwater algae that has anti-inflammatory and antiaging activity; however, its effects on ultraviolet-damaged skin have yet to be elucidated. This study investigated the antiapoptosis and wound-healing effects of loliolide using HaCaT cells (a human keratinocyte cell line). Loliolide inhibited the expression of reactive oxygen species (ROS) induced by ultraviolet radiation as well as wrinkle formation-related matrix metalloproteinase genes and increased the expression of the damage repair-related gene SIRT1. The apoptosis signaling pathway was confirmed by Western blot analysis, which showed that loliolide was able to reduce the expression of caspases 3, 8, and 9, which are related to ROS-induced apoptosis. In addition, Western blotting, reverse-transcription polymerase chain reaction (PCR), and real-time PCR analyses showed that loliolide enhanced the expression of the epidermal growth factor receptor signaling pathway (PI3K, AKT) and migration factors, such as K6, K16, and K17; keratinocyte growth factor; and inflammatory cytokines, such as interleukin (IL)-1, IL-17, and IL-22 expressed during the cellular scratching process, suggesting a putative wound-healing ability. Because of the antiapoptosis and antiscratching effects on skin of both loliolide and loliolide-rich Prasiola japonica ethanol extract, we consider the former to be an important compound used in the cosmeceutical industry.

In Vitro Photoprotective, Anti-Inflammatory, Moisturizing, and Antimelanogenic Effects of a Methanolic Extract of Chrysophyllum lucentifolium Cronquist.

UVB exposure causes DNA mutation and ROS generation, which lead to skin photoaging, skin wrinkling, skin sagging, and uneven skin pigmentation. ROS activate the NF-κB and MAPK signaling pathways leading to production of inflammatory molecules such as COX-2, collagen-degrading proteins such as matrix metalloproteinases (MMPs), and moisture-deficiency-related proteins such as hyaluronidases (HYALs). UVB exposure also induces irregular skin pigmentation though melanin overproduction, related to CREB transcription factor activity and transcription of melanogenesis genes. Here, we demonstrate that Chrysophyllum lucentifolium methanol extract (Cl-ME) has antioxidant activity; it dose-dependently decreased the expression of COX-2, MMP-1, MMP-9, HYAL-1, and HYAL-4 by downregulating the NF-κB (IKKα/ß, IκBα) and MAPK (ERK, JNK, and p38) pathways and increased the expression of Col1a1, which encodes a protein important for maintaining skin elasticity. Cl-ME also showed promising antimelanogenic activity by decreasing the expression of CREB, a transcription factor, which in turn inhibited the expression of genes encoding tyrosinase, MITF, TYRP1, and TYRP2. In summary, a methanol extract of C. lucentifolium exhibited antiphotoaging and antimelanogenic activity and could be useful in the cosmeceutical industry.

Medicinal potential of Panax ginseng and its ginsenosides in atopic dermatitis treatment.

Atopic dermatitis (AD) is a chronic and relapsing inflammatory disease that affects 1%-20% of people worldwide. Despite affecting many people, AD current treatments, such as corticosteroids and calcineurin inhibitors, have not only harmful secondary effects but are also often ineffective. Therefore, natural nontoxic compounds are on high demand for developing new effective AD treatments. Panax ginseng Meyer has been used traditionally for its promising healing and restorative properties to treat many diseases including skin disorders, reason why in this review we want to explore the research performed with AD and P. ginseng as well as determining its potential for new drug development. Previous researches have shown that P. ginseng has positive effects in AD patients such as lower eczema area and severity index, transepidermal water loss, and immunoglobulin E levels and better quality of sleep. In vivo animal models, as well, have shown positive results to P. ginseng and derived ginsenosides, such as the decrease of transepidermal water loss, immunoglobulin E levels in serum, allergy-related cytokines, and downregulation of NF-κB, MAPK, and Ikaros pathways. All of these previous data suggest that P. ginseng and its derived ginsenosides are undoubtedly a nontoxic effective option to treat AD.

Panax ginseng-derived fraction BIOGF1K reduces atopic dermatitis responses via suppression of mitogen-activated protein kinase signaling pathway.

BACKGROUND: BIOGF1K, a fraction of Panax ginseng, has desirable antimelanogenic, anti-inflammatory, and antiphotoaging properties that could be useful for treating skin conditions. Because its potential positive effects on allergic reactions in skin have not yet been described in detail, this study's main objective was to determine its efficacy in the treatment of atopic dermatitis (AD). METHODS: High-performance liquid chromatography was used to verify the compounds in BIOGF1K, and we used the (3-4-5-dimethylthiazol-2-yl)-2-5-diphenyltetrazolium bromide method to determine its cytotoxicity in RBL-2H3 and HMC-1 cell lines. RBL-2H3 cells were induced using both anti-DNP-IgE/DNP-BSA and calcium ionophore (A2187) treatments, whereas HMC-1 cells were induced using A2187 alone. To measure mast cell degranulation, we performed histamine (enzyme-linked immunosorbent assay) and ß-hexosaminidase assays. To quantify interleukin (IL)-4, IL-5, and IL-13 levels in RBL-2H3 cells, we performed quantitative polymerase chain reaction (PCR); to quantify expression levels of IL-4 and IL-13 in HMC-1 cells, we used semiquantitative reverse transcription polymerase chain reaction (RT-PCR). Finally, we detected the total and phosphorylated forms of extracellular signal-regulated kinase, p-38, and c-Jun N-terminal kinase proteins by immunoblotting. RESULTS: BIOGF1K decreased the AD response by reducing both histamine and ß-hexosaminidase release as well as reducing the secretion levels of IL-4, IL-5, and IL-13 in RBL-2H3 cells and IL-4 and IL-13 in HMC-1 cells. In addition, BIOGF1K decreased MAPK pathway activation in RBL-2H3 and HMC-1 cells. CONCLUSIONS: BIOGF1K attenuated the AD response, hence supporting its use as a promising and natural approach for treating AD.

Viburnum pichinchense methanol extract exerts anti-inflammatory effects via targeting the NF-κB and caspase-11 non-canonical inflammasome pathways in macrophages.

ETHNOPHARMACOLOGICAL RELEVANCE: Viburnum pichinchense Benth. Mainly found in Ecuador and Colombia has been ethnopharmacologically utilized as a remedy for various female disorders with kidney inflammation and uterine relaxant. AIM OF THE STUDY: The pharmacological activity of Viburnum pichinchense has never been studied, therefore, this study explored anti-inflammatory activity of Viburnum pichinchense methanol extract (Vp-ME). MATERIALS AND METHODS: Anti-inflammatory activities of Vp-ME were evaluated in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and HCl/EtOH-induced gastritis mice by MTT assay, nitric oxide (NO) production assay, semi-quantitative reverse-transcriptase-polymerase chain reaction (RT-PCR), luciferase reporter assay, Western blotting, and enzyme-linked immunosorbent assays (ELISA). Anti-inflammatory compounds in Vp-ME were identified by high performance liquid chromatography (HPLC). RESULTS: Vp-ME inhibited NO production in RAW264.7 cells stimulated with pam3CSK4, poly I:C or LPS and in LPS-stimulated peritoneal macrophages without cytotoxicity and downregulated mRNA expression of inflammatory enzymes, inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) and pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and IL-6. The anti-inflammatory activity was accomplished by inhibiting nuclear factor-kappa B (NF-κB) transcriptional activation, upstream signaling molecules in the NF-κB pathway, and caspase-11 non-canonical inflammasome in RAW264.7 cells. Moreover, Vp-ME exhibited in vivo anti-inflammatory activity by ameliorating gastritis symptoms, inhibiting iNOS and IL-6 mRNA expression and IκBα activation in mice. HPLC analysis identified resveratrol, quercetin, luteolin, and kaempferol as the anti-inflammatory components in Vp-ME. CONCLUSION: This study demonstrated Vp-ME has the anti-inflammatory activity via targeting NF-κB and caspase-11 non-canonical inflammasome pathways in macrophage-mediated inflammatory responses, suggesting Vp-ME could be developed as anti-inflammatory ethnopharmacological remedies to prevent and treat inflammatory diseases.