scholarly journals Standardized Edible Bird's Nest Extract Prevents UVB Irradiation-Mediated Oxidative Stress and Photoaging in the Skin

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1452
Author(s):  
Ok-Kyung Kim ◽  
Dakyung Kim ◽  
Minhee Lee ◽  
Seong-Hoo Park ◽  
Wakana Yamada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ultraviolet B ◽  
Type I ◽  
Ceramide Synthase ◽  
Hairless Mice ◽  
In Vivo Models ◽  
Uvb Irradiation ◽  
Edible Bird’S Nest

We investigated whether standardized edible bird’s nest extract (BNE-PK) can prevent ultraviolet B (UVB) irradiation-mediated oxidative stress and photoaging in the skin using in vitro and in vivo models. BNE-PK increased skin hydration by hyaluronic acid synthesis and activation of ceramide synthase in UVB-irradiated hairless mice and HaCaT cells. Furthermore, BNE-PK suppressed melanogenesis by down-regulation of the cAMP/PKA/CREB/MITF/TRP-1/TRP-2/tyrosinase pathway in UVB-irradiated hairless mice and 3-isobutyl-1-methylxanthine (IBMX)-treated B16F10 cells. In UVB-irradiated hairless mice, BNE-PK attenuated the wrinkle formation-related JNK/c-FOS/c-Jun/MMP pathway and activated the TGF-βRI/SMAD3/pro-collagen type I pathway during UVB-mediated oxidative stress. Based on these findings, our data suggest that BNE-PK may potentially be used for the development of effective natural anti-photoaging functional foods for skin health.

Photoprotection of maqui berry against ultraviolet B-induced photodamage in vitro and in vivo

2020 ◽  
Vol 11 (3) ◽  
pp. 2749-2762 ◽  
Author(s):  
Ling Chen ◽  
Gao Zhou ◽  
Xiao-Shan Meng ◽  
Hui-Ying Fu ◽  
Qi-Gui Mo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Ultraviolet B ◽  
Uvb Irradiation ◽  
Maqui Berry ◽  
Berry Extracts ◽  
Cellular Dna

Maqui berry extracts could ameliorate oxidative stress, cellular DNA damage, and inflammation induced by UVB-irradiation in vitro and in vivo.

scholarly journals Vascular Dysfunction Induced by Mercury Exposure

2019 ◽  
Vol 20 (10) ◽  
pp. 2435 ◽  
Author(s):  
Tetsuya Takahashi ◽  
Takayoshi Shimohata
Keyword(s):  
Oxidative Stress ◽  
Vascular Dysfunction ◽  
Brain Parenchyma ◽  
Transport Systems ◽  
Mehg Exposure ◽  
In Vivo Models ◽  
The Central Nervous System ◽  
The Brain

Methylmercury (MeHg) causes severe damage to the central nervous system, and there is increasing evidence of the association between MeHg exposure and vascular dysfunction, hemorrhage, and edema in the brain, but not in other organs of patients with acute MeHg intoxication. These observations suggest that MeHg possibly causes blood–brain barrier (BBB) damage. MeHg penetrates the BBB into the brain parenchyma via active transport systems, mainly the l-type amino acid transporter 1, on endothelial cell membranes. Recently, exposure to mercury has significantly increased. Numerous reports suggest that long-term low-level MeHg exposure can impair endothelial function and increase the risks of cardiovascular disease. The most widely reported mechanism of MeHg toxicity is oxidative stress and related pathways, such as neuroinflammation. BBB dysfunction has been suggested by both in vitro and in vivo models of MeHg intoxication. Therapy targeted at both maintaining the BBB and suppressing oxidative stress may represent a promising therapeutic strategy for MeHg intoxication. This paper reviews studies on the relationship between MeHg exposure and vascular dysfunction, with a special emphasis on the BBB.

scholarly journals Inflammation and Oxidative Stress in Diabetic Kidney Disease: The Targets for SGLT2 Inhibitors and GLP-1 Receptor Agonists

2021 ◽  
Vol 22 (19) ◽  
pp. 10822
Author(s):  
Agata Winiarska ◽  
Monika Knysak ◽  
Katarzyna Nabrdalik ◽  
Janusz Gumprecht ◽  
Tomasz Stompór
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Kidney Injury ◽  
Organ Protection ◽  
In Vivo Models ◽  
Diabetic Kidney ◽  
And Oxidative Stress

The incidence of type 2 diabetes (T2D) has been increasing worldwide, and diabetic kidney disease (DKD) remains one of the leading long-term complications of T2D. Several lines of evidence indicate that glucose-lowering agents prevent the onset and progression of DKD in its early stages but are of limited efficacy in later stages of DKD. However, sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor (GLP-1R) antagonists were shown to exert nephroprotective effects in patients with established DKD, i.e., those who had a reduced glomerular filtration rate. These effects cannot be solely attributed to the improved metabolic control of diabetes. In our review, we attempted to discuss the interactions of both groups of agents with inflammation and oxidative stress—the key pathways contributing to organ damage in the course of diabetes. SGLT2i and GLP-1R antagonists attenuate inflammation and oxidative stress in experimental in vitro and in vivo models of DKD in several ways. In addition, we have described experiments showing the same protective mechanisms as found in DKD in non-diabetic kidney injury models as well as in some tissues and organs other than the kidney. The interaction between both drug groups, inflammation and oxidative stress appears to have a universal mechanism of organ protection in diabetes and other diseases.

scholarly journals Oral Intake of Collagen Peptide Attenuates Ultraviolet B Irradiation-Induced Skin Dehydration In Vivo by Regulating Hyaluronic Acid Synthesis

2018 ◽  
Vol 19 (11) ◽  
pp. 3551 ◽  
Author(s):  
Min Kang ◽  
Silvia Yumnam ◽  
Sun Kim
Keyword(s):  
Hyaluronic Acid ◽  
Oral Administration ◽  
Protein Expression ◽  
Ultraviolet B ◽  
Skin Hydration ◽  
Skin Barrier Function ◽  
Hairless Mice ◽  
Uvb Irradiation ◽  
Collagen Peptide

Collagen peptide (CP) has beneficial effects on functions of the skin, such as skin barrier function and skin elasticity, in vivo. However, there are few studies investigating the mechanism underlying the potential effects of CP in skin epidermal moisturization after ultraviolet B (UVB) irradiation. In this study, we examined whether orally-administered CP affects the loss of skin hydration induced by UVB irradiation in hairless mice. SKH-1 hairless mice were orally administered CP at two doses (500 and 1000 mg/kg) for nine weeks, and the dorsal skin was exposed to UVB. The potential effects of CP were evaluated by measuring the transepidermal water loss (TEWL), skin hydration, wrinkle formation, and hyaluronic acid expression in the dorsal mice skin. We found that oral administration of CP increased skin hydration and decreased wrinkle formation compared to the UVB-irradiated group. Treatment of CP increased the mRNA and protein expression of hyaluronic acid synthases (HAS-1 and -2) concomitant with an increased hyaluronic acid production in skin tissue. The expression of hyaluronidase (HYAL-1 and 2) mRNA was downregulated in the CP-treated group. In addition, the protein expression of skin-hydrating factors, filaggrin and involucrin, was upregulated via oral administration of CP. In summary, these results show that oral administration of CP increases hyaluronic acid levels, which decreases during UVB photoaging. Therefore, we suggest that CP can be used as a nutricosmetic ingredient with potential effects on UVB-induced skin dehydration and moisture loss in addition to wrinkle formation.

scholarly journals In Vitro and In Vivo Inhibitory Effect of Citrus Junos Tanaka Peel Extract against Oxidative Stress-Induced Apoptotic Death of Lung Cells

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1231
Author(s):  
Jin Woo Kim ◽  
Eun Hee Jo ◽  
Ji Eun Moon ◽  
Hanvit Cha ◽  
Moon Han Chang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Inhibitory Effect ◽  
Lung Cells ◽  
In Vivo Models ◽  
Citrus Junos ◽  
Induced Apoptosis ◽  
Peel Extract

Various stresses derived from both internal and external oxidative environments lead to the excessive production of reactive oxygen species (ROS) causing progressive intracellular oxidative damage and ultimately cell death. The objective of this study was to evaluate the protective effects of Citrus junos Tanaka peel extract (CE) against oxidative-stress induced the apoptosis of lung cells and the associated mechanisms of action using in vitro and in vivo models. The protective effect of CE was evaluated in vitro in NCI-H460 human lung cells exposed to pro-oxidant H2O2. The preventive effect of CE (200 mg/kg/day, 10 days) against pulmonary injuries following acrolein inhalation (10 ppm for 12 h) was investigated using an in vivo mouse model. Herein, we demonstrated the inhibitory effect of CE against the oxidative stress-induced apoptosis of lung cells under a highly oxidative environment. The function of CE is linked with its ability to suppress ROS-dependent, p53-mediated apoptotic signaling. Furthermore, we evaluated the protective role of CE against apoptotic pulmonary injuries associated with the inhalation of acrolein, a ubiquitous and highly oxidizing environmental respiratory pollutant, through the attenuation of oxidative stress. The results indicated that CE exhibits a protective effect against the oxidative stress-induced apoptosis of lung cells in both in vitro and in vivo models.

scholarly journals Ocular Delivery of Polyphenols: Meeting the Unmet Needs

Molecules ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 370
Author(s):  
Luna Krstić ◽  
María J. González-García ◽  
Yolanda Diebold
Keyword(s):  
Oxidative Stress ◽  
Polyphenolic Compounds ◽  
In Vivo Models ◽  
Structural Peculiarities ◽  
Inflammatory Processes ◽  
Delivery Strategies ◽  
Low Solubility ◽  
Ocular Therapy

Nature has become one of the main sources of exploration for researchers that search for new potential molecules to be used in therapy. Polyphenols are emerging as a class of compounds that have attracted the attention of pharmaceutical and biomedical scientists. Thanks to their structural peculiarities, polyphenolic compounds are characterized as good scavengers of free radical species. This, among other medicinal effects, permits them to interfere with different molecular pathways that are involved in the inflammatory process. Unfortunately, many compounds of this class possess low solubility in aqueous solvents and low stability. Ocular pathologies are spread worldwide. It is estimated that every individual at least once in their lifetime experiences some kind of eye disorder. Oxidative stress or inflammatory processes are the basic etiological mechanisms of many ocular pathologies. A variety of polyphenolic compounds have been proved to be efficient in suppressing some of the indicators of these pathologies in in vitro and in vivo models. Further application of polyphenolic compounds in ocular therapy lacks an adequate formulation approach. Therefore, more emphasis should be put in advanced delivery strategies that will overcome the limits of the delivery site as well as the ones related to the polyphenols in use. This review analyzes different drug delivery strategies that are employed for the formulation of polyphenolic compounds when used to treat ocular pathologies related to oxidative stress and inflammation.

Probiotic yeast Kluyveromyces marxianus CIDCA 8154 shows anti-inflammatory and anti-oxidative stress properties in in vivo models

2016 ◽  
Vol 7 (1) ◽  
pp. 83-93 ◽  
Author(s):  
D.E. Romanin ◽  
S. Llopis ◽  
S. Genovés ◽  
P. Martorell ◽  
V.D. Ramón ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kluyveromyces Marxianus ◽  
Intestinal Inflammation ◽  
In Vivo Models ◽  
Benzene Sulfonic Acid ◽  
Bowel Diseases ◽  
Probiotic Yeast ◽  
Anti Inflammatory

Inflammatory bowel diseases (IBDs) are complex affections with increasing incidence worldwide. Multiple factors are involved in the development and maintenance of the symptoms including enhanced oxidative stress in intestinal mucosa. The conventional therapeutic approaches for IBDs are based on the use anti-inflammatory drugs with important collateral effects and partial efficacy. In the present work we tested the anti-inflammatory capacity of Kluyveromyces marxianus CIDCA 8154 in different models. In vitro, we showed that the pretreatment of epithelial cells with the yeast reduce the levels of intracellular reactive oxygen species. Furthermore, in a murine model of trinitro benzene sulfonic acid-induced colitis, yeast-treated animals showed a reduced histopathological score (P<0.05) and lower levels of circulating interleukin 6 (P<0.05). The capacity to modulate oxidative stress in vivo was assessed using a Caenorhabditis elegans model. The yeast was able to protect the nematodes from oxidative stress by modulating the SKN-1 transcription factor trough the DAF-2 pathway. These results indicate that K. marxianus CIDCA 8154 could control the intestinal inflammation and cellular oxidative stress. Deciphering the mechanisms of action of different probiotics might be useful for the rational formulation of polymicrobial products containing microorganisms targeting different anti-inflammatory pathways.

scholarly journals The Involvement of Mycobacterium Type III-A CRISPR-Cas System in Oxidative Stress

2021 ◽  
Vol 12 ◽  
Author(s):  
Fan Yang ◽  
Lingqing Xu ◽  
Lujie Liang ◽  
Wanfei Liang ◽  
Jiachen Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Envelope ◽  
Reduction Process ◽  
Intracellular Survival ◽  
Host Immunity ◽  
Type I ◽  
Type Iii

Type I and type II CRISPR-Cas systems are employed to evade host immunity by targeting interference of bacteria’s own genes. Although Mycobacterium tuberculosis (M. tuberculosis), the causative agent of tuberculosis, possesses integrated type III-A CRISPR-Cas system, its role in mycobacteria remains obscure. Here, we observed that seven cas genes (csm2∼5, cas10, cas6) were upregulated in Mycobacterium bovis BCG under oxidative stress treatment, indicating the role of type III-A CRISPR-Cas system in oxidative stress. To explore the functional role of type III-A CRISPR-Cas system, TCC (Type III-A CRISPR-Cas system, including cas6, cas10, and csm2-6) mutant was generated. Deletion of TCC results in increased sensitivity in response to hydrogen peroxide and reduced cell envelope integrity. Analysis of RNA-seq dataset revealed that TCC impacted on the oxidation-reduction process and the composition of cell wall which is essential for mycobacterial envelop integrity. Moreover, disrupting TCC led to poor intracellular survival in vivo and in vitro. Finally, we showed for the first time that TCC contributed to the regulation of regulatory T cell population, supporting a role of TCC in modulating host immunity. Our finding reveals the important role of TCC in cell envelop homeostasis. Our work also highlights type III-A CRISPR-Cas system as an important factor for intracellular survival and host immunoregulation in mycobacteria, thus may be a potential target for therapy.

scholarly journals Chloroquine and Gemifloxacin Potentiate the Anticancer Effect of Doxorubicin: In-Vitro and In-Vivo Models

2019 ◽  
Vol 12 (04) ◽  
pp. 1613-1620
Author(s):  
Sahar Ezeldien ◽  
Waleed F Khalil ◽  
Mostafa Fayez ◽  
Mohamed M. Abdel-Daim
Keyword(s):  
Oxidative Stress ◽  
Cell Lines ◽  
Hematological Parameters ◽  
In Vivo Models ◽  
Doxorubicin Treatment ◽  
Blood Biochemical ◽  
Antitumor Properties ◽  
A549 Lung

Doxorubicin is one of the most effective anthracycline anticancer drugs, but it causes several adverse effects. Our study was designed to assess the consequences of combining doxorubicin with chloroquine or gemifloxacin. Drugs cytotoxicity was assessed on two different cell lines; A549 lung adenocarcinoma and MCF7 breast cancer. The in-vitro oxidative stress was also measured. In the in-vivo experiment, Ehrlich ascetis carcinoma-bearing mice, different treatments with doxorubicin, chloroquine, gemifloxacin and their combinations were evaluated. Survival indices (MST and ILS%) and blood biochemical parameters as well as the histopathological picture were studied. Results showed that, doxorubicin combinations were more cytotoxic on MCF7 and A549 cell lines than doxorubicin alone. The combinations significantly decreased the oxidative stress resulted from doxorubicin treatment. Furthermore, these combinations improved hematological parameters and histopathological pictures in the treated mice. In conclusion, chloroquine and gemifloxacin significantly enhance the antitumor properties of doxorubicin and reduce its toxicity.

scholarly journals Acidic Phospholipase A2-Peptide Derivative Modulates Oxidative Status and Microstructural Reorganization of Scar Tissue after Cutaneous Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Estefanny Ruiz García ◽  
Edvaldo Barros ◽  
Stephanie Stransky ◽  
Carlos Chávez-Olórtegui ◽  
Mariella Bontempo Freitas ◽  
...  
Keyword(s):  
Phospholipase A2 ◽  
Scar Tissue ◽  
Oxidative Status ◽  
Time Dependent ◽  
Type I ◽  
Potential Candidate ◽  
In Vivo Models ◽  
Carbonyl Protein

From in vitro and in vivo models, the proliferative and healing potential of an acidic phospholipase A2 (LAPLA2) from Lachesis muta venom was investigated. The LAPLA2 proliferative activity was evaluated on fibroblasts and keratinocytes cultured, and the antioxidant and regenerative potential of LAPLA2 was analyzed in a murine model. The animal study consisted of four groups: C (negative control): 0.9% NaCl; SS (positive control): 1% silver sulfadiazine; L1 group: 0.5% LAPLA2; and L2 group: 0.25% LAPLA2. Wounds were topically treated daily for 12 days, and scar tissue samples were collected every 4 days. In vitro, LAPLA2 stimulated marked time-dependent cell proliferation. In vivo, it increased the antioxidant activity of superoxide dismutase (SOD) and catalase (CAT) and decreased malondialdehyde (MDA) and carbonyl protein (CP) levels in scar tissue treated with LAPLA2 at 0.5%. This peptide was effective in stimulating cellular proliferation, neoangiogenesis, type I and III collagen deposition, and maturation in a time-dependent-way, reducing the time required for wound closure. Our results indicated that LAPLA2 presented a remarkable potential in improving the oxidative status and microstructural reorganization of the scar tissue by stimulation of cellularity, angiogenesis, colagenogenesis, and wound contraction, suggesting that the peptide could be a potential candidate for a new healing drug.

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