Advances in Extraction Technologies of Silybum marianum L. and Its Role in Protecting Against Skin Damage

Genetic Alteration of Keap1 Confers Constitutive Nrf2 Activation and Resistance to Chemotherapy in Gallbladder Cancer

Inhibition of cytochrome P450 2E1 and activation of transcription factor Nrf2 are renoprotective in myoglobinuric acute kidney injury

Exposing skin to ultraviolet (UV) radiation contributes to photoaging and to the development of skin cancer by DNA lesions and triggering inflammatory and other harmful cellular cascades. The present study tested the ability of unique lipid molecules, polyhydroxylated fatty alcohols (PFA), extracted from avocado, to reduce UVB-induced damage and inflammation in skin. Introducing PFA to keratinocytes prior to their exposure to UVB exerted a protective effect, increasing cell viability, decreasing the secretion of IL-6 and PGE(2), and enhancing DNA repair. In human skin explants, treating with PFA reduced significantly UV-induced cellular damage. These results support the idea that PFA can play an important role as a photo-protective agent in UV-induced skin damage.

Epidermal growth factor (EGF) plays an important role in corneal epithelial migration and proliferation to improve the wound healing process. This study aimed to understand the role of NFκB in EGF-induced corneal epithelial wound healing through regulation of CTCF activity, which plays important roles in cell motility and migration to promote wound healing. The effect of NFκB p50 on corneal epithelial wound healing was investigated by comparing the eyes of wild-type and p50 knockout mice. We found that there was a significant retardation in corneal epithelial wound healing in the corneas of p50 knockout mice. Wound closure rates were measured in human corneal epithelial cells transfected with an NFκB activation-sensitive CTCF expression construct to demonstrate the effect of human CTCF expression under the control of EGF-induced NFκB activation on wound healing. EGF stimulation activated NFκB, which directly triggered the expression of the exogenous human CTCF in transfected cells and, subsequently, promoted human corneal epithelial cell motility, migration, and wound healing. Overexpression of CTCF in corneal epithelial cells and mouse corneas significantly enhanced the wound healing process. Furthermore, the effect of overexpressing NFκB p50 in corneal epithelial cells on the promotion of wound healing was abolished by knockdown of CTCF with CTCF-specific shRNA. Thus, a direct regulatory relationship between EGF-induced NFκB p50 and CTCF activation affecting corneal epithelial wound healing has been established, indicating that CTCF is, indeed, a NFκB p50-targeted and effective gene product in the core transcriptional network downstream from the growth factor-induced NFκB signaling pathway.

Non-melanoma skin cancer (NMSC) accounts for >1 million new cases each year in the US alone suggesting that more approaches are needed for its prevention and control. Earlier studies by us have shown that silymarin (a crude form of biologically active silibinin with some other isomers), isolated from milk thistle, affords strong protection against ultraviolet (UV) radiation-induced NMSC in SKH-1 hairless mice; however, the molecular mechanisms of its efficacy are not known. Here, we assessed the effect of silibinin on UV-induced DNA damage and p53-p21/Cip1 accumulation, and their roles in UV-induced cell proliferation and apoptosis in SKH-1 hairless mouse epidermis. Topical application of silibinin prior to, or immediately after, UV irradiation resulted in a very strong protective effect against UV-induced thymine dimer positive cells in epidermis accounting for 76-85% (P < 0.001) inhibition. In other studies, silibinin treatment resulted in a further up-regulation of p53 by approximately 1.6-fold (P < 0.001) together with an increase ( approximately 2-fold, P < 0.001) in p21/Cip1 protein levels. Proliferative cell nuclear antigen staining showed that silibinin pre- or post-topical application significantly inhibits (40-52 and 20-40%, respectively, P < 0.001) UV-induced epidermal cell proliferation. In addition, silibinin strongly decreased UV-caused terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive apoptotic/sunburn cell formation (P < 0.001). These findings suggest that silibinin affords strong protection against UV-induced damage in epidermis by a decrease in thymine dimer positive cells and an up-regulation of p53-p21/Cip1 possibly leading to an inhibition in both cell proliferation and apoptosis. Comparable effects of silibinin following its pre- or post-UV application suggest that mechanisms other than sunscreen effect are operational in silibinin efficacy against UV-caused skin damages.

Melatonin and roentgen irradiation of the testis

α-MSH-Stimulated Tolerogenic Dendritic Cells Induce Functional Regulatory T Cells and Ameliorate Ongoing Skin Inflammation

Cellular therapy may be the solution of challenging problems in colorectal surgery such as impaired healing leading to anastomotic leakage and metastatic colorectal cancer (CRC). This review aimed to illustrate the role of cellular therapy in promotion of wound healing and management of metastatic CRC. An organized literature search for the role of cellular therapy in promotion of wound healing and management of metastatic CRC was conducted. Electronic databases including PubMed/Medline, Scopus, and Embase were queried for the search process. Two types of cellular therapy have been recognized, the mesenchymal stem cells (MSCs) and bone marrow-mononuclear cells (BM-MNCs) therapy. These cells have been shown to accelerate and promote healing of various tissue injuries in animal and human studies. In addition, experimental studies have reported that MSCs may help suppress the progression of colon cancer in rat models. This article reviews the possible mechanisms of action and clinical utility of MSCs and BM-MNCs in promotion of healing and suppression of tumor growth in light of the published literature. Cellular therapy has a potentially important role in colorectal surgery, particularly in the promotion of wound healing and management of metastatic CRC. Future directions of cellular therapy in colorectal surgery were explored which may help stimulate futures studies on the role of cellular therapy in colorectal surgery.

Enzyme-Independent NO Stores in Human Skin: Quantification and Influence of UV Radiation

Dietary Lutein/Zeaxanthin Decreases Ultraviolet B-Induced Epidermal Hyperproliferation and Acute Inflammation in Hairless Mice

Reply to Letter: Skin and soft tissue damage caused by use of feedback sensor during chest compressions

Learning How to Believe: Epistemic Development in Cultural Context

Aspirin’s Protective Effects Highlight the Role of Inflammation in UV-Induced Skin Damage and Carcinogenesis

A role for Zn(2+) in accelerating wound healing is established, yet, the signaling pathways linking Zn(2+) to tissue repair are not well known. We show that in the human HaCaT keratinocytes extracellular Zn(2+) induces a metabotropic Ca(2+) response that is abolished by silencing the expression of the G-protein-coupled receptor GPR39, suggesting that this Zn(2+)-sensing receptor, ZnR, is mediating the response. Keratinocytic-ZnR signaling is highly selective for Zn(2+) and can be triggered by nanomolar concentrations of this ion. Interestingly, Zn(2+) was also released following cellular injury, as monitored by a specific non-permeable fluorescent Zn(2+) probe, ZnAF-2. Chelation of Zn(2+) and scavenging of ATP from conditioned medium, collected from injured epithelial cultures, was sufficient to eliminate the metabotropic Ca(2+) signaling. The signaling triggered by Zn(2+), via ZnR, or by ATP further activated MAP kinase and induced up-regulation of the sodium/proton exchanger NHE1 activity. Finally, activation of ZnR/GPR39 signaling or application of ATP enhanced keratinocytes scratch closure in an in vitro model. Thus our results indicate that extracellular Zn(2+), which is either applied or released following injury, activates ZnR/GPR39 to promote signaling leading to epithelial repair.

Intravenously Injected Human Fibroblasts Home to Skin Wounds, Deliver Type VII Collagen, and Promote Wound Healing