Evaluation of Chemical, Antipsoriatic and Antiangiogenic Properties of Salt from Lonar Crater Lake Water

2019 ◽  
Vol 4 (3) ◽  
pp. 159-165
Author(s):  
Prakash Bansode ◽  
Indumathi Somasundaram ◽  
Apurva Birajdar ◽  
Sanjay Mishra ◽  
Dhanashree Patil ◽  
...  
Keyword(s):  
Lake Water ◽  
Crater Lake ◽  
Skin Diseases ◽  
Therapeutic Potential ◽  
Chorioallantoic Membrane ◽  
Soda Lake ◽  
Antiangiogenic Activity ◽  
The Impact ◽  
Lonar Crater

Lonar Crater lake was created by the impact of a massive meteor during the Pleistocene Epoch. Being a hypersaline and hyperalkaline soda lake, rich microbial diversity is reported earlier. Lonar lake water is used by local people and tribals against skin diseases. These observations prompted us to investigate the therapeutic potential of lake water against skin diseases. In this context, we have conducted pilot study to assess the antipsoriatic and antiangiogenic activity of the salt obtained from lake water using THP1 cell line by MTT assay and antiangiogenic activity by in vivo chicken chorioallantoic membrane (CAM) assay, as there is a close relation between psoriasis and angiogenesis. The results revealed that salt possess remarkable antipsoriatic and antiangiogenic activity.

scholarly journals S1P Increases VEGF Production in Osteoblasts and Facilitates Endothelial Progenitor Cell Angiogenesis by Inhibiting miR-16-5p Expression via the c-Src/FAK Signaling Pathway in Rheumatoid Arthritis

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2168
Author(s):  
Chien-Chung Huang ◽  
Tzu-Ting Tseng ◽  
Shan-Chi Liu ◽  
Yen-You Lin ◽  
Yat-Yin Law ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Therapeutic Potential ◽  
Chorioallantoic Membrane ◽  
Tube Formation ◽  
In Vivo Model ◽  
Endothelial Progenitor ◽  
Chick Chorioallantoic Membrane ◽  
Cartilage Erosion ◽  
The Impact

Angiogenesis is a critical process in the formation of new capillaries and a key participant in rheumatoid arthritis (RA) pathogenesis. Vascular endothelial growth factor (VEGF) stimulation of endothelial progenitor cells (EPCs) facilitates angiogenesis and the progression of RA. Phosphorylation of sphingosine kinase 1 (SphK1) produces sphingosine-1-phosphate (S1P), which increases inflammatory cytokine production, although the role of S1P in RA angiogenesis is unclear. In this study, we evaluated the impact of S1P treatment on VEGF-dependent angiogenesis in osteoblast-like cells (MG-63 cells) and the significance of SphK1 short hairpin RNA (shRNA) on S1P production in an in vivo model. We found significantly higher levels of S1P and VEGF expression in synovial fluid from RA patients compared with those with osteoarthritis by ELISA analysis. Treating MG-63 cells with S1P increased VEGF production, while focal adhesion kinase (FAK) and Src siRNAs and inhibitors decreased VEGF production in S1P-treated MG-63 cells. Conditioned medium from S1P-treated osteoblasts significantly increased EPC tube formation and migration by inhibiting miR-16-5p synthesis via proto-oncogene tyrosine-protein kinase src (c-Src) and FAK signaling in chick chorioallantoic membrane (CAM) and Matrigel plug assays. Infection with SphK1 shRNA reduced angiogenesis, articular swelling and cartilage erosion in the ankle joints of mice with collagen-induced arthritis (CIA). S1P appears to have therapeutic potential in RA treatment.

scholarly journals Nanoformulation Shows Cytotoxicity against Glioblastoma Cell Lines and Antiangiogenic Activity in Chicken Chorioallantoic Membrane

Pharmaceutics ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 862
Author(s):  
Danieli Rosane Dallemole ◽  
Thatiana Terroso ◽  
Aline de Cristo Soares Alves ◽  
Juliete Nathali Scholl ◽  
Giovana Ravizzoni Onzi ◽  
...  
Keyword(s):  
Cell Lines ◽  
Therapeutic Potential ◽  
Chorioallantoic Membrane ◽  
Spherical Shape ◽  
Control Treatment ◽  
Phase Cell ◽  
Antiangiogenic Activity ◽  
Chicken Chorioallantoic Membrane

Glioblastoma (GB) is a histological and genetically heterogeneous brain tumor that is highly proliferative and vascularized. The prognosis is poor with currently available treatment. In this study, we evaluated the cytotoxicity and antiangiogenic activity of doxorubicin-loaded-chitosan-coated-arginylglycylaspartic acid-functionalized-poly(ε-caprolactone)-alpha bisabolol-LNC (AB-DOX-LNC-L-C-RGD). The nanoformulation was prepared by self-assembling followed by interfacial reactions, physicochemically characterized and evaluated in vitro against GB cell lines (U87MG and U138MG) and in vivo using the chicken chorioallantoic membrane assay (CAM). Spherical shape nanocapsules had a hydrodynamic mean diameter of 138 nm, zeta potential of +13.4 mV, doxorubicin encapsulation of 65%, and RGD conjugation of 92%. After 24 h of treatment (U87MG and U138MG), the median inhibition concentrations (IC50) were 520 and 490 nmol L−1 doxorubicin-equivalent concentrations, respectively. The treatment induced antiproliferative activity with S-phase cell-cycle arrest and apoptosis in the GB cells. Furthermore, after 48 h of exposure, evaluation of antiangiogenic activity (CAM) showed that the relative vessel growth following treatment with the nanocapsules was 5.4 times lower than that with the control treatment. The results support the therapeutic potential of the nanoformulation against GB and, thereby, pave the way for future preclinical studies.

scholarly journals Insights into Host–Pathogen Interactions in Biofilm-Infected Wounds Reveal Possibilities for New Treatment Strategies

Antibiotics ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 396
Author(s):  
Hannah Trøstrup ◽  
Anne Sofie Boe Laulund ◽  
Claus Moser
Keyword(s):  
Wound Healing ◽  
Host Response ◽  
Chronic Wounds ◽  
Therapeutic Potential ◽  
Recent Observation ◽  
Treatment Strategies ◽  
Normal Wound Healing ◽  
Inflammatory Phase ◽  
The Impact

Normal wound healing occurs in three phases—the inflammatory, the proliferative, and the remodeling phase. Chronic wounds are, for unknown reasons, arrested in the inflammatory phase. Bacterial biofilms may cause chronicity by arresting healing in the inflammatory state by mechanisms not fully understood. Pseudomonas aeruginosa, a common wound pathogen with remarkable abilities in avoiding host defense and developing microbial resistance by biofilm formation, is detrimental to wound healing in clinical studies. The host response towards P. aeruginosa biofilm-infection in chronic wounds and impact on wound healing is discussed and compared to our own results in a chronic murine wound model. The impact of P. aeruginosa biofilms can be described by determining alterations in the inflammatory response, growth factor profile, and count of leukocytes in blood. P. aeruginosa biofilms are capable of reducing the host response to the infection, despite a continuously sustained inflammatory reaction and resulting local tissue damage. A recent observation of in vivo synergism between immunomodulatory and antimicrobial S100A8/A9 and ciprofloxacin suggests its possible future therapeutic potential.

scholarly journals Degradation of Mitochondria and Oxidative Stress as the Main Mechanism of Toxicity of Pristine Graphene on U87 Glioblastoma Cells and Tumors and HS-5 Cells

2019 ◽  
Vol 20 (3) ◽  
pp. 650 ◽  
Author(s):  
Sławomir Jaworski ◽  
Barbara Strojny ◽  
Ewa Sawosz ◽  
Mateusz Wierzbicki ◽  
Marta Grodzik ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Chorioallantoic Membrane ◽  
In Vivo Model ◽  
Pristine Graphene ◽  
Infrared Measurements ◽  
The Impact

Due to the development of nanotechnologies, graphene and graphene-based nanomaterials have attracted immense scientific interest owing to their extraordinary properties. Graphene can be used in many fields, including biomedicine. To date, little is known about the impact graphene may have on human health in the case of intentional exposure. The present study was carried out on U87 glioma cells and non-cancer HS-5 cell lines as in vitro model and U87 tumors cultured on chicken embryo chorioallantoic membrane as in vivo model, on which the effects of pristine graphene platelets (GPs) were evaluated. The investigation consisted of structural analysis of GPs using transmission electron microscopy, Fourier transmission infrared measurements, zeta potential measurements, evaluation of cell morphology, assessment of cell viability, investigation of reactive oxygen species production, and investigation of mitochondrial membrane potential. The toxicity of U87 glioma tumors was evaluated by calculating the weight and volume of tumors and performing analyses of the ultrastructure, histology, and protein expression. The in vitro results indicate that GPs have dose-dependent cytotoxicity via ROS overproduction and depletion of the mitochondrial membrane potential. The mass and volume of tumors were reduced in vivo after injection of GPs. Additionally, the level of apoptotic and necrotic markers increased in GPs-treated tumors.

scholarly journals DAPK1 loss triggers tumor invasion in colorectal tumor cells

2019 ◽  
Vol 10 (12) ◽  
Author(s):  
Sara Steinmann ◽  
Philipp Kunze ◽  
Chuanpit Hampel ◽  
Markus Eckstein ◽  
Jesper Bertram Bramsen ◽  
...  
Keyword(s):  
Chorioallantoic Membrane ◽  
Gene Expression Signature ◽  
Predictive Biomarker ◽  
Cancer Type ◽  
Potential Candidate ◽  
Metastatic Progression ◽  
Death Associated Protein Kinase ◽  
The Impact

AbstractColorectal cancer (CRC) is one of the leading cancer-related causes of death worldwide. Despite the improvement of surgical and chemotherapeutic treatments, as of yet, the disease has not been overcome due to metastasis to distant organs. Hence, it is of great relevance to understand the mechanisms responsible for metastasis initiation and progression and to identify novel metastatic markers for a higher chance of preventing the metastatic disease. The Death-associated protein kinase 1 (DAPK1), recently, has been shown to be a potential candidate for regulating metastasis in CRC. Hence, the aim of the study was to investigate the impact of DAPK1 protein on CRC aggressiveness. Using CRISPR/Cas9 technology, we generated DAPK1-deficient HCT116 monoclonal cell lines and characterized their knockout phenotype in vitro and in vivo. We show that loss of DAPK1 implemented changes in growth pattern and enhanced tumor budding in vivo in the chorioallantoic membrane (CAM) model. Further, we observed more tumor cell dissemination into chicken embryo organs and increased invasion capacity using rat brain 3D in vitro model. The novel identified DAPK1-loss gene expression signature showed a stroma typical pattern and was associated with a gained ability for remodeling the extracellular matrix. Finally, we suggest the DAPK1-ERK1 signaling axis being involved in metastatic progression of CRC. Our results highlight DAPK1 as an anti-metastatic player in CRC and suggest DAPK1 as a potential predictive biomarker for this cancer type.

Pharmacologic Replacement of BIM BH3 Reactivates Apoptosis in Hematologic Cancer and Lymphoproliferative Disease.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 524-524
Author(s):  
James L. LaBelle ◽  
Jill K. Fisher ◽  
Samuel G. Katz ◽  
Gregory H. Bird ◽  
Chelsea E. Lawrence ◽  
...  
Keyword(s):  
Cell Death ◽  
Mouse Models ◽  
Therapeutic Potential ◽  
Control Point ◽  
Lymphoproliferative Disease ◽  
Critical Control Point ◽  
Hematologic Cancer ◽  
Apoptotic Proteins ◽  
The Impact

Abstract Selective targeting of deregulated apoptotic protein networks is a promising pharmacologic strategy for subverting diseases of unrestrained cellular survival, such as cancer. BCL-2 family protein interactions constitute a critical control point for the regulation of apoptosis. Whereas multidomain anti-apoptotic proteins such as BCL-2 guard against cell death, multidomain pro-apoptotic proteins such as BAX constitute a gateway to cell death through mitochondrial damage. The BH3-only proteins function as death sentinels situated throughout the cell, poised to transmit signals of cellular injury to multidomain members. BH3-only proteins deliver their death messages via their conserved alpha-helical BH3 domains. Whereas the indirect activator class of BH3-only proteins (e.g. BAD) counteract anti-apoptotic proteins, the direct activator subgroup (e.g. BIM) is believed to trigger apoptosis both by neutralizing anti-apoptotics and by directly activating the mitochondrial executioners BAX and BAK. The essential roles of BH3-only proteins in maintaining cellular homeostasis is highlighted by the development of autoimmune disease and cancer in mouse models of BH3-only protein deficiency. By inserting hydrocarbon “staples” into native BH3 peptide sequences, we have produced a chemical toolbox of stabilized alpha-helices of BCL-2 domains (SAHBs) to dissect apoptotic signaling pathways in vivo and explore the pharmacodynamic effects of “BH3 replacement” in cancer cells and mouse models of deregulated apoptosis. Whereas SAHBs display high affinity binding to anti-apoptotic targets, BID and BIM SAHBs also directly engage BAX and are thus especially potent in inducing apoptosis of a panel of leukemia and lymphoma cell lines. To evaluate the impact of selective BH3 replacement in vivo, we tested the capacity of BIM SAHB to reactivate apoptosis in the lymphoproliferative disease of Bim-/- mice. Strikingly, Bim-/- mice treated with BIM SAHB displayed marked influx of tingible-body macrophages into the lymphoid infiltrates of affected organs, with scattered cells throughout the infiltrate robustly positive for activated caspase-3, suggestive of SAHB induced apoptosis induction. Our studies highlight the therapeutic potential of BH3 replacement to circumvent apoptotic blockade and restore the death pathway in hematologic cancer and lymphoproliferative disease.

scholarly journals Cannabis sativa and Skin Health: Dissecting the Role of Phytocannabinoids

Planta Medica ◽  
2021 ◽  
Author(s):  
Giulia Martinelli ◽  
Andrea Magnavacca ◽  
Marco Fumagalli ◽  
Mario DellʼAgli ◽  
Stefano Piazza ◽  
...  
Keyword(s):  
Clinical Studies ◽  
Skin Diseases ◽  
Cannabis Sativa ◽  
Therapeutic Potential ◽  
Current Evidence ◽  
Skin Disorders ◽  
Anti Inflammatory

AbstractThe use of Cannabis sativa is currently recognized to ease certain types of chronic pain, reduce chemotherapy-induced nausea, and improve anxiety. Nevertheless, few studies highlighted the therapeutic potential of C. sativa extracts and related phytocannabinoids for a variety of widespread skin disorders including acne, atopic dermatitis, psoriasis, pruritus, and pain. This review summarized the current evidence on the effects of phytocannabinoids at the cutaneous level through the collection of in vitro, in vivo, and clinical studies published on PubMed, Scopus, Embase, and Web of Science until October 2020. Phytocannabinoids have demonstrated potential anti-inflammatory, antioxidant, anti-aging, and anti-acne properties by various mechanisms involving either CB1/2-dependent and independent pathways. Not only classical immune cells, but also several skin-specific actors, such as keratinocytes, fibroblasts, melanocytes, and sebocytes, may represent a target for phytocannabinoids. Cannabidiol, the most investigated compound, revealed photoprotective, antioxidant, and anti-inflammatory mechanisms at the cutaneous level, while the possible impact on cell differentiation, especially in the case of psoriasis, would require further investigation. Animal models and pilot clinical studies supported the application of cannabidiol in inflammatory-based skin diseases. Also, one of the most promising applications of non-psychotropic phytocannabinoids is the treatment of seborrheic disorders, especially acne. In conclusion, the incomplete knowledge of the role of the endocannabinoid system in skin disorders emerged as an important limit for pharmacological investigations. Moreover, the limited studies conducted on C. sativa extracts suggested a higher potency than single phytocannabinoids, thus stimulating new research on phytocannabinoid interaction.

scholarly journals Mesenchymal Stromal Cells From Emphysematous Donors and Their Extracellular Vesicles Are Unable to Reverse Cardiorespiratory Dysfunction in Experimental Severe Emphysema

2021 ◽  
Vol 9 ◽  
Author(s):  
Mariana A. Antunes ◽  
Cassia L. Braga ◽  
Tainá B. Oliveira ◽  
Jamil Z. Kitoko ◽  
Ligia L. Castro ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Therapeutic Potential ◽  
Chronic Obstructive ◽  
Severe Emphysema ◽  
Arginase 1 ◽  
The Impact

Although bone marrow-derived mesenchymal stromal cells (BM-MSCs) from patients with chronic obstructive pulmonary disease (COPD) appear to be phenotypically and functionally similar to BM-MSCs from healthy sources in vitro, the impact of COPD on MSC metabolism and mitochondrial function has not been evaluated. In this study, we aimed to comparatively characterize MSCs from healthy and emphysematous donors (H-MSCs and E-MSCs) in vitro and to assess the therapeutic potential of these MSCs and their extracellular vesicles (H-EVs and E-EVs) in an in vivo model of severe emphysema. For this purpose, C57BL/6 mice received intratracheal porcine pancreatic elastase once weekly for 4 weeks to induce emphysema; control animals received saline under the same protocol. Twenty-four hours after the last instillation, animals received saline, H-MSCs, E-MSCs, H-EVs, or E-EVs intravenously. In vitro characterization demonstrated that E-MSCs present downregulation of anti-inflammatory (TSG-6, VEGF, TGF-β, and HGF) and anti-oxidant (CAT, SOD, Nrf2, and GSH) genes, and their EVs had larger median diameter and lower average concentration. Compared with H-MSC, E-MSC mitochondria also exhibited a higher respiration rate, were morphologically elongated, expressed less dynamin-related protein-1, and produced more superoxide. When co-cultured with alveolar macrophages, both H-MSCs and E-MSCs induced an increase in iNOS and arginase-1 levels, but only H-MSCs and their EVs were able to enhance IL-10 levels. In vivo, emphysematous mice treated with E-MSCs or E-EVs demonstrated no amelioration in cardiorespiratory dysfunction. On the other hand, H-EVs, but not H-MSCs, were able to reduce the neutrophil count, the mean linear intercept, and IL-1β and TGF-β levels in lung tissue, as well as reduce pulmonary arterial hypertension and increase the right ventricular area in a murine model of elastase-induced severe emphysema. In conclusion, E-MSCs and E-EVs were unable to reverse cardiorespiratory dysfunction, whereas H-EVs administration was associated with a reduction in cardiovascular and respiratory damage in experimental severe emphysema.

scholarly journals Chronic sodium bromide relieves autistic-like deficits in the Oprm1 mouse model of autism and modulates the activity of serotonin and dopamine receptors in vitro

2020 ◽  
Author(s):  
Cécile Derieux ◽  
Sébastien Roux ◽  
Thierry Plouvier ◽  
Audrey Léauté ◽  
Agathe Brugoux ◽  
...  
Keyword(s):  
Mouse Model ◽  
Dopamine Receptors ◽  
Therapeutic Potential ◽  
Autism Spectrum ◽  
Chloride Ions ◽  
Sodium Bromide ◽  
Bromide Ion ◽  
The Impact

Chronic sodium bromide relieves autistic-like deficits in the Oprm1 mouse model of autism and modulates the activity of serotonin and dopamine receptors in vitro C. DERIEUX 1 , S. ROUX 1 , A. LEAUTE 1 , T. PLOUVIER 2 , J.A.J. BECKER 1 , J. LE MERRER 1 1 Déficits de Récompense, GPCRs et Sociabilité, Physiologie de la Reproduction et des Comportements, INRA UMR0085, CNRS UMR7247, Université de Tours, Inserm ; 37380 Nouzilly, France 2 Térali Innov, 37230 Fondettes, France Corresponding author : [email protected] Autism spectrum disorders (ASD) are complex neurodevelopmental diseases whose diagnosis lies on the detection of impaired social skills together with restricted and repetitive behavior and interests (DSM-5). Although the etiology of ASD remains mostly unknown, impaired excitation/inhibition ratio appears as a common mechanistic feature. Bromide ion is known to reduce hyperexcitability, possibly by competing with chloride ions at channels and transporters and may thus have therapeutic potential in ASD. Aims : We evaluated the therapeutic potential of bromide ion in the Oprm1 -/- mouse model of ASD and the molecular mechanisms involved in bromide treatment, notably effects on GPCRs. Methods : In vivo , we first assessed the effect of chronically administered sodium bromide on autistic-like behavioral deficits and performed RT-qPCR on brain structures known to be involved in ASD. In vitro , we evaluated the impact of bromide ion on G-protein mediated signaling of serotonin and dopamine receptors. Results : In vivo , sodium bromide (30 to 500 mg/Kg) dose-dependently improved social interaction and preference, reduced stereotypies and decreased anxiety. Bromide also impacts the expression of genes coding for some GPCRs, chloride transporters and GABA A subunits. In vitro , bromide behaves as a positive allosteric modulator of 5-HT 6 , 5-HT 7 and D1 receptors but not 5-HT 4 and D2 receptors. Conclusions : The beneficial effects of bromide administration in a genetic murine model of ASD and its impact on both gene expression and GPCR pharmacology predicts high translational potential in patients with autism, despite high heterogeneity in etiology and symptoms.

scholarly journals Designing of Chitosan Derivatives Nanoparticles with Antiangiogenic Effect for Cancer Therapy

Nanomaterials ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 698
Author(s):  
Oana-Maria Dragostin ◽  
Rodica Tatia ◽  
Sangram Keshari Samal ◽  
Anca Oancea ◽  
Alexandra Simona Zamfir ◽  
...  
Keyword(s):  
Cancer Therapy ◽  
Tumor Cells ◽  
Therapeutic Potential ◽  
Antioxidant Properties ◽  
Chorioallantoic Membrane ◽  
Cancer Therapies ◽  
Antiangiogenic Effect ◽  
Chitosan Derivatives

Angiogenesis is a physiological process involving the growth of new blood vessels, which provides oxygen and required nutrients for the development of various pathological conditions. In a tumor microenvironment, this process upregulates the growth and proliferation of tumor cells, thus any stage of angiogenesis can be a potential target for cancer therapies. In the present study, chitosan and his derivatives have been used to design novel polymer-based nanoparticles. The therapeutic potential of these newly designed nanoparticles has been evaluated. The antioxidant and MTT assays were performed to know the antioxidant properties and their biocompatibility. The in vivo antiangiogenic properties of the nanoparticles were evaluated by using a chick Chorioallantoic Membrane (CAM) model. The obtained results demonstrate that chitosan derivatives-based nanostructures strongly enhance the therapeutic effect compared to chitosan alone, which also correlates with antitumor activity, demonstrated by the in vitro MTT assay on human epithelial cervical Hep-2 tumor cells. This study opens up new direction for the use of the chitosan derivatives-based nanoparticles for designing of antiangiogenic nanostructured materials, for future cancer therapy.

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