Current Issue : April - June Volume : 2018 Issue Number : 2 Articles : 5 Articles
Pathogenesis of AKI is complex and involves both local events in the kidney as well as systemic effects in the body that are\ninterconnected and interdependent. Despite intensive investigations there is still no pharmacological agent that could provide\ncomplete protection against cisplatin nephrotoxicity. In the last decade mesenchymal stem cells (MSCs) have been proposed as a\npotentially useful therapeutic strategy in various diseases, including acute kidney injury. Although MSCs have potent\nimmunosuppressive properties, animal studies also suggest that transplanted MSCs may elicit immune response. Interestingly,\ntumorigenicity of transplanted MSCs in animal studies has been rarely studied. Since the risk of tumorigenicity of particular\ntherapy as well as the immune response to solid or cell grafts is a major issue in clinical trials, the aim of the present paper is to\ncritically summarize the results of MSC transplantation on animal models of AKI, particularly cisplatin-induced animal models,\nand to expose results and main concerns about immunogenicity and tumorigenicity of transplanted MSCs, two important issues\nthat need to be addressed in future studies....
Oxidative stress plays a crucial role in the salivary gland dysfunction in insulin resistance (IR). It is not surprising that new\nsubstances are constantly being sought that will protect against the harmful effects of IR in the oral cavity environment. The\npurpose of this study was to evaluate the effect of N-acetylcysteine (NAC) on oxidative stress and secretory function of salivary\nglands in a rat model of insulin resistance. Rats were divided into 4 groups: Cââ?¬â?normal diet, C +NACââ?¬â?normal diet + NAC,\nHFDââ?¬â?high-fat diet, and HFD+ NAC. We have demonstrated that NAC elevated enzymatic (superoxide dismutase, catalase,\nand peroxidase) and nonenzymatic antioxidants (reduced glutathione (GSH) and total antioxidant capacity (TAS)) in the\nparotid glands of HFD +NAC rats, while in the submandibular glands increased only GSH and TAS levels. NAC protects\nagainst oxidative damage only in the parotid glands and increased stimulated salivary secretion; however, it does not increase\nthe protein secretion in the both salivary glands. Summarizing, NAC supplementation prevents the decrease of stimulated saliva\nsecretion, seen in the HFD rats affected. NAC improves the antioxidative capacity of the both glands and protects against\noxidative damage to the parotid glands of IR rats....
Lycium barbarum polysaccharide (LBP) is themajor function component of Lycium barbarum L. and has been previously reported\nto induce the phenotypic and functionalmaturation of dendritic cells (DCs) aswell as activating T lymphocytes. In the current study,\nthe immunologic cytotoxicity promoting effect of LBP was assessed and the underlying mechanism was explored. The impact of\nLBP on the phenotype, maturation, and immunogenicity of DCs was assessed. The activity of Notch pathway which is involved\nin the regulation of LBP on DCs was detected. Afterwards, the influence of LBP on cytotoxicity of DC-mediated cytotoxicity T\nlymphocytes (CTLs) to CT26-WT colon cancer cells was further assessed. Administration of LBP induced the phenotypic and\nfunctional maturation of DCs. After being subjected to LBP, the expression of Notch and Jagged and Notch targets Hes1 and Hes5\nwas all upregulated. The cytotoxicity of DC-mediated CTLs was strengthened by administration of LBP. Additionally, cytotoxicity\nof DC-mediated CTLs on CT26-WT colon cancer cells also increased with effector-target ratio. In conclusion, LBP could induce\nthe phenotypic and functional maturation of DCs via Notch signaling and promote the cytotoxicity of DC-mediated CTLs, which\ncould be employed as a promising adjuvant for cancer immunotherapy....
Background. Cigarette smoke (CS) induces an oxidative stress, DNA damage, and lung cancer. Pomegranate juice (PJ) possess\npotent antioxidant activity attributed to its polyphenols. We investigated whether PJ supplementation would prevent the\nformation of lung nodules, attenuate mitotic activity, and reduce hypoxia-inducible factor-1�± (HIF-1�±) expression secondary\nto CS exposure in an animal model. Methods. Mice were divided into: Control group, CS group, CS + PJ group, and PJonly\ngroup. CS and CS + PJ were exposed to CS, 5 days per week, for a total of 5 months. Animals were then housed for\nadditional four months. CS + PJ and PJ groups received PJ throughout the experiment period while others received placebo. At\nthe end of the experiment, the incidence of lung nodules was assessed by (1) histological analysis, (2) mitotic activity\n[measurement of PHH3 antibodies], and (3) measurement of HIF-1�± expression. Results. The incidence of lung nodules was\nsignificantly increased in CS. CS exposure significantly increased PHH3 and HIF-1�± expression. PJ supplementation attenuated\nthe formation of lung nodules and reduced PHH3 and HIF-1�± expression. Conclusion. PJ supplementation significantly\ndecreased the incidence of lung cancer, secondary to CS, prevented the formation of lung nodules, and reduced mitotic activity\nand HIF-1�± expression in an animal model....
Surgical flaps are frequently affected by ischemia/reperfusion (I/R) injury. Calcium-sensing receptor (CaSR) and stromal cellderived\nfactor-1�±) are closely associated with myocardial I/R injury.This study was performed to evaluate the feasibility\nof applying SDF-1�± to counteract CaSR activation-mediated I/R injury in ischemic free flaps. Free flaps that underwent ischemia\nfor 3 h were equally randomized into five groups: CaCl2, NPS2143 + CaCl2, SDF-1�± + CaCl2, AMD3100 + SDF-1�± + CaCl2, and\nnormal saline. The free flaps were harvested to evaluate flap necrosis and neovascularization after 2 h or 7 d of reperfusion. p-\nCaSR/CaSR was extensively expressed in vascular endothelial cells of free flaps after I/R injury, andactivation of the SDF-1�± /CXCR4\naxis and NPS2143 could reduce the expression of cleaved caspase-3, caspase-9, FAS, Cyt-c, and Bax and increase Bcl-2 expression;\nthe opposite was true after CaSR activation. Interestingly, initiation of the SDF-1�± /CXCR4 axis might abrogate CaSR activationinduced\nI/R injury through enhancement of microvessel density. In conclusion, CaSR might become a novel therapeutic target of\nfree flaps affected by I/R injury. Activation of the SDF-1�±/CXCR4 axis and NPS2143 could counteract CaSR activation-mediated\nI/R injury and promote free flap survival through inhibition of caspase-3/caspase-9-related cell apoptosis and enhancement of\nneovascularization....
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