Hot Water Extract of Sasa borealis (Hack.) Makino & Shibata Abate Hydrogen Peroxide-Induced Oxidative Stress and Apoptosis in Kidney Epithelial Cells.

Sasa borealis (Hack.) Makino & Shibata or broad-leaf bamboo is famous for its richness of bioactive natural products and its uses in traditional medicine for its anti-inflammatory, diuretic, and antipyretic properties and preventive effects against hypertension, arteriosclerosis, cardiovascular disease, and cancer. The present study investigated the antioxidant activity of S. borealis hot water extract (SBH) and its effects in ameliorating hydrogen peroxide-induced oxidative stress, using an African green monkey kidney epithelial cell line (Vero). Known polyphenols in SBH were quantified by HPLC analysis. SBH indicated a dose-dependent increase for reducing power, ABTS+ (IC50 = 96.44 ± 0.61 µg/mL) and DPPH (IC50 = 125.78 ± 4.41 µg/mL) radical scavenging activities. SBH markedly reduced intracellular reactive oxygen species (ROS) generation in the Vero cells and increased the protective effects against H2O2-induced oxidative stress by reducing apoptosis. Other than the direct involvement in neutralizing ROS, metabolites in SBH were also found to induce NRF2-mediated production of antioxidant enzymes, HO-1, and NQO1. These findings imply that S. borealis hot water extract can be utilized to create nutraceutical and functional foods that can help to relieve the effects of oxidative stress in both acute and chronic kidney injury.

(-)-Loliolide Isolated from Sargassum horneri Abate UVB-Induced Oxidative Damage in Human Dermal Fibroblasts and Subside ECM Degradation.

Ultraviolet (UV) B exposure is a prominent cause of skin aging and a contemporary subject of interest. The effects are progressing through the generation of reactive oxygen species (ROS) that alter cell signaling pathways related to inflammatory responses. The present study evaluates the protective effects of (7aR)-6-hydroxy-4,4,7a-trimethyl-6,7-dihydro-5H-1-benzofuran-2-one (HTT) isolated from the edible brown algae Sargassum horneri against UVB protective effects in human dermal fibroblasts (HDFs). HTT treatment dose-dependently suppressed intracellular ROS generation in HDFs with an IC50 of 62.43 ± 3.22 µM. HTT abated UVB-induced mitochondrial hyperpolarization and apoptotic body formation. Furthermore, UVB-induced activation of key nuclear factor (NF)-κB and mitogen-activated protein kinase signaling proteins were suppressed in HTT treated cells while downregulating pro-inflammatory cytokines (interleukin-1ß, 6, 8, 33 and tumor necrosis factor-α). Moreover, HTT treatment downregulated matrix metalloproteinase1, 2, 3, 8, 9 and 13 that was further confirmed by the inhibition of collagenase and elastase activity. The evidence implies that HTT delivers protective effects against premature skin aging caused by UVB exposure via suppressing inflammatory responses and degradation of extracellular matrix (ECM) components. Extensive research in this regard will raise perspectives for using HTT as an ingredient in UV protective ointments.

UVB protective effects of Sargassum horneri through the regulation of Nrf2 mediated antioxidant mechanism.

The present study aimed to evaluate the protective effect of a methanol extract of Sargassum horneri (SHM), which contains 6-hydroxy-4,4,7a-trimethyl-5,6,7,7a-tetrahydrobenzofuran-2(4H)-one (HTT) and apo-9'-fucoxanthinone, against ultraviolet B (UVB)-induced cellular damage in human keratinocytes and its underlying mechanism. SHM significantly improved cell viability of UVB-exposed human keratinocytes by reducing the generation of intracellular reactive oxygen species (ROS). Moreover, SHM inhibited UVB exposure-induced apoptosis by reducing the formation of apoptotic bodies and the populations of the sub-G1 hypodiploid cells and the early apoptotic cells by modulating the expression of the anti- and pro-apoptotic molecules, Bcl-2 and Bax, respectively. Furthermore, SHM inhibited NF-κB p65 activation by inducing the activation of Nrf2/HO-1 signaling. The cytoprotective and antiapoptotic activities of SHM are abolished by the inhibition of HO-1 signaling. In further study, SHM restored the skin dryness and skin barrier disruption in UVB-exposed human keratinocytes. Based to these results, our study suggests that SHM protects the cells against UVB-induced cellular damages through the Nrf2/HO-1/NF-κB p65 signaling pathway and may be potentially useful for the prevention of UVB-induced skin damage.

Sargassum horneri (Turner) C. Agardh ethanol extract attenuates fine dust-induced inflammatory responses and impaired skin barrier functions in HaCaT keratinocytes.

ETHNOPHARMACOLOGICAL RELEVANCE: Sargassum horneri (Turner) C. Agardh is well known in East Asia as an edible brown alga rich in bioactive compounds. It has an ethnopharmacological significance in traditional Chinese medicine to treat inflammatory disorders varying from edema, furuncles, dysuria to cardiovascular diseases. AIM OF THE STUDY: Surge of fine dust (FD), in densely populated areas, have been reported to cause adverse health conditions ranging from respiratory diseases to inflammatory skin disorders. The current study investigates the protective effects of an ethanol extract from S. horneri (SHE) on FD-induced inflammatory responses and impaired skin hydration in HaCaT keratinocytes. MATERIALS AND METHODS: Intracellular reactive oxygen species (ROS) generation was evaluated with the 2',7'-Dichlorofluorescin diacetate (DCFH-DA) stain. Anti-inflammatory properties of SHE in FD-stimulated HaCaT keratinocytes were investigated for the suppression of nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) pathways and downregulation of pro-inflammatory cytokines. As a means of studying FD-induced skin barrier disruption and the effects of SHE on stratum corneum hydration-controlling factors, tight junction regulatory mediators, and hyaluronic acid (HA) production were evaluated using keratinocytes. RESULTS: SHE suppressed the intracellular ROS production, simultaneously improving cell viability in FD-stimulated keratinocytes. Also, SHE upregulated anti-inflammatory cytokine interleukin (IL)-4 while downregulating inflammatory cytokines IL-1ß, IL-6, IL-8, tumor necrosis factor (TNF)-α; epidermal and epithelial cytokines IL-25, IL-33, and thymic stromal lymphopoietin (TSLP); thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC) and regulated upon activation, normally T-expressed, and presumably secreted expression and suppressed (RANTES) chemokine, MAPK and NF-κB mediators in a dose-dependent manner. Furthermore, SHE ameliorated filaggrin, involucrin, lymphoepithelial Kazal-type-related inhibitor (LEKTI), signifying its beneficial effects on deteriorated skin hydration caused by FD-induced inflammation. SHE further exhibited its skin protective effects regulating the tight junction proteins; Occludin, zonula occludens (ZO)-1, claudin-1, claudin-4, claudin-7, and claudin-23 while increasing the production of HA minimizing skin damage. CONCLUSIONS: Anti-inflammatory effects of, SHE against FD-induced keratinocyte inflammation is attributable to the suppression of upstream MAPK and NF-κB mediators. SHE indicated potential anti-inflammatory properties attenuating deteriorated skin barrier function in HaCaT keratinocytes. The effects are attributable to the polyphenols and other antioxidant compounds in SHE. Further studies could envisage the use of SHE for developing rejuvenating cosmetics.

Oral Administration of Sargassum horneri Improves the HDM/DNCB-Induced Atopic Dermatitis in NC/Nga Mice.

The present study investigated the protective effects of Sargassum horneri (S. horneri) ethanol extract (SHE) against atopic dermatitis (AD), known as an abnormal immune response in house dust mite (HDM)/2,4-dinitrochlorobenzene (DNCB)-stimulated NC/Nga mice. The oral administration of SHE attenuated the AD symptoms, including the skin dermatitis severity, transepidermal water loss (TEWL), and ear edema in HDM/DNCB-stimulated mice. Moreover, the histological analysis revealed that SHE improved epidermal hyperplasia and hyperkeratosis, and reduced the dermal infiltrations of mast cells and eosinophils. Moreover, SHE downregulated the expression levels of cytokines (interleukin (IL)-6, IL-10, and interferon (IFN)-γ) and chemokines (Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES), Eotaxin, and Thymus and activation-regulated chemokine (TARC)) by decreasing the expression levels of atopic initiators (IL-25 and IL-33) in HDM/DNCB-stimulated skin. The oral administration of SHE decreased the spleen size, reducing expression levels of AD-related cytokines (IL-4, IL-5, IL-6, IL-10, IL-13, IFN-γ, and TARC) by regulating the expressions of Tbx21 (T-bet), GATA Binding Protein 3 (GATA-3), and Signal transducer and activator of transcription 3 (STAT3). Moreover, SHE significantly attenuated the serum immunoglobulin (Ig)G1 and IgG2a levels in HDM/DNCB-stimulated mice. Collectively, these results suggest that S. horneri could be an ingredient of functional food against abnormal immune response.

Step gradient alcohol precipitation for the purification of low molecular weight fucoidan from Sargassum siliquastrum and its UVB protective effects.

Ultraviolet B (UVB) can induce oxidative damage to outermost layers of skin causing suntans, sunburns, and, in severe cases, blisters leading to photoaging. Low molecular weight (MW) fucoidan is renowned for possessing enhanced antioxidant activities. The present study discloses the use of step gradient ethanol precipitation in refining fucoidan fractions (SSQC1-SSQC4) from Sargassum siliquastrum and evaluation of their UVB-protective effects in human HaCaT keratinocytes. Among the fractions, SSQC4 indicated the best bioactive effects. 1H NMR, FTIR, monosaccharide composition by HPAEC-PAD analysis, MW estimation by agarose gel electrophoresis were used to characterize the fractions. SSQC4 was comprising of fucoidan, with an estimated MW distribution of 8-25 kDa. Exposure of UVB increased intracellular ROS, DNA damage, loss of mitochondrial membrane potential, apoptotic body formation causing cell death through the mitochondria-mediated apoptosis pathway. SSQC4 treatment could dose-dependently attenuate the ROS levels and suppress mitochondria-mediated apoptosis in UVB exposed keratinocytes. SSQC4 treatment enhanced cellular antioxidant defense by increasing Nrf2 mediated HO-1 generation, which was identified as the cause of observed bioactivities. The safety and stability of SSQC4 could be further evaluated to promote its use as a bioactive natural ingredient in UV-protective cosmetics.