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Cell-based therapies using mesenchymal stem cells provide hopeful results. Therefore, in this present study, possible anti-inflammatory and anti-nociceptive actions of locally or systemically treated adipose-derived mesenchymal stem cells (ADMSCs) investigated in experimental inflammation model. ADMSCs were isolated from a male Wistar rat under anesthesia, and then they were cultured and expanded for transplantation in all the experimental animals. Effects of intraperitoneal or intraplantar ADMSC treatments on the hallmarks of the inflammatory nociception, such as hyperalgesia, allodynia, edema, and several biochemical parameters were investigated using a well-established carrageenan (CG)-induced hindpaw inflammation model in male rats. Both local and systemic ADMSC treatment increased the latencies, thresholds, and the development of edema in a time-dependent manner. In addition, administration of ADMSC suppressed the increased level of interleukin (IL)-1β, IL-6, and nitric oxide (NO), but further enhanced that of IL-10. Locally treated ADMSC at inflammatory sites effectively suppressed the CG-induced inflammatory responses when compared to the intraperitoneal route of administration. Findings suggest that therapeutic potential of ADMSC can change depending on its route of administration. Local ADMSC treatments may suppress the development of inflammatory-nociception and edema by decreasing the production of pro-inflammatory cytokines and NO level and increasing the anti-inflammatory cytokine production at inflammatory sites.

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Abstract. Estrogen mediates fast signal responses or transcriptional events via G protein-coupled estrogen receptor 1 (GPER1). However, there is no data on the effect of GPER1 on lung cancer cell proliferation and apoptosis. The present study aimed to analyze the anticancer effects of the GPER1 agonist G-1 on A549 human lung cancer cells. A549 cells were treated with 17β-estradiol and G-1, and cell proliferation was analyzed using MTT and WST assays. In addition, the apoptotic effects induced by G-1 were investigated using acridine orange/ethidium bromide staining. A549 cells were treated with a half maximal inhibitory concentration of G-1 for 72 h, and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) enzyme activities were analyzed by spectrophotometry. The results revealed that G-1 significantly decreased cell proliferation. In addition to the antiprolif erative effect of G-1, a marked increase in apoptotic activity was observed when cells were treated with 2x10-5 M G-1. Furthermore, G-1 increased NO levels, and SOD and GPx activity. These findings indicate that the GPER1 agonist G-1 is able to exert antiproliferative and proapoptotic effects on A549 cells, and that oxidant and antioxidant molecules may mediate these effects.

CAPE has a protective effect on ARPE-19 cells against oxidative stress, and VEGF protein level and expression can be decreased by incubation with different concentrations of CAPE. These results demonstrate that CAPE suppresses the mitochondria-mediated apoptosis in ARPE-19 cells under oxidative stress. In addition, the use of CAPE in combination with bevacizumab has an additive effect.