Previous studies have reported that 4,6′-Anhydrooxysporidinone (SSF2-2), isolated from Fusarium lateritium SSF2, has neuroprotective effects on the HT-22 hippocampal neuronal cell line. However, the anti-cancer effect of SSF2-2 remains unclear. Here, we examined the viability of MCF-7 human breast cancer cells treated with SSF2-2 or left untreated using a cell viability assay kit. The underlying molecular mechanism was further investigated by Western blotting and immunocytochemistry studies. The results demonstrated that SSF2-2 inhibited the viability of MCF-7 cells. Treatment with SSF2-2 increased the levels of cleaved caspase-9, cleaved caspase-7, poly (ADP-ribose) polymerase (PARP), and LC3B. Additionally, SSF2-2 significantly increased the conversion of LC3-I to LC3II and LC3-positive puncta in MCF-7 cells.
Objectives: This study was conducted to evaluate the effects of Pueraria lobata (PL) extract on obesity related hormones in rats with estrogen deficiency. Methods: The experiments were performed with the use of ovariectomized rats as estrogen-deficient obesity rat model. They were grouped Normal (sham operation group), Control (ovariectomy group), 50 mg/kg PL (ovariectomy group+50 mg/kg of PL), 100 mg/kg PL (ovariectomy group+100 mg/kg of PL), 200 mg/kg PL (ovariectomy group+200 mg/kg of PL). PL extract was orally administered for 8 weeks once a day. Body weights and serum levels of hormones, such as leptin, estradiol, cholecystokinin (CCK), ghrelin, and adiponectin were estimated by ELISA. Results: PL extract significantly decreased body weight, the serum levels of leptin in estrogen-deficient obesity rats. PL extract significantly increased the serum levels of estradiol and CCK. However, PL extract did not directly effect on the levels of ghrelin and adiponectin in estrogen-deficient obesity rats. Conclusions: It is concluded that PL extract reduced body weight, and regulate the hormones related to energy metabolism. PL extract decreased the serum levels of leptin. PL extract increased the serum levels of estradiol and CCK. These results indicate that PL might have potentials for treatment of obesity and complications during the menopause caused by estrogen-deficiency.
Background and Objectives: Korean red ginseng (KRG) is known as an immune-enhancing health food and has been approved by the Korea Food and Drug Administration. We analyzed the immune-enhancing activity of KRG and its polysaccharide (KRG-P) using RAW264.7 murine macrophage cells. Materials and Methods: The protein and mRNA expression levels of IL-6 and TNF-α were measured using ELISA and qRT-PCR, respectively. Nitric oxide levels were measured using the Griess reagent. The phosphorylation and total protein levels of ERK, p38, JNK, p65, and GAPDH were determined by immunoblot assay. Results: The polysaccharide (KRG-P), but not KRG, produced nitric oxide, interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α) in RAW 264.7 cells. KRG-P increased nitric oxide synthase 2 (NOS2), IL-6, and TNF-α expression in RAW264.7 cells. KRG-P also increased phosphorylation of MAPKs (mitogen-activate protein kinases) including ERK, p38, JNK, and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) in a concentration-dependent manner in RAW264.7 cells. Conclusions: The polysaccharide KRG-P is the active component responsible for the immune-enhancing activity of Korean red ginseng and may modulate the systemic immune system in vivo.
[Hypothesis] The present study sought to investigate the in vitro and in vivo anticancer effect of two representative omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), with a focus on assessing the role of fatty acid-induced oxidative stress and apoptosis as mechanisms for their anticancer actions. [Methods] We used in vitro cell culture of MCF-7 human breast cancer cells and in vivo athymic nude mice model to study the effect of omega-3 fatty acids on cancer cell proliferation and the mechanism of the cell death. [Results] In vitro studies showed that DHA and EPA each strongly reduced the viability and DNA synthesis of MCF-7 human breast cancer cells in culture, and they also promoted cell death via apoptosis. Mechanistically, accumulation of reactive oxygen species and activation of caspase 8 contributed critically to the induction of apoptotic cell death. Co-presence of antioxidants or a selective inhibition or knockdown of caspase 8 each effectively abrogated the cytotoxic effect of DHA. Using athymic nude mice as an in vivo model, we found that feeding animals with 5% fish oil-containing diet for 6 weeks significantly reduced the growth of MCF-7 human breast cancer cells through inhibition of cancer cell proliferation as well as promotion of cell death. Using 3-nitrotyrosine as a parameter, we confirmed that fish oil diet significantly increased oxidative stress in tumor cells in vivo. Analysis of fatty acid content in plasma and tissues showed that feeding animals a 5% fish oil diet significantly increased DHA and EPA levels in both normal and tumorous mammary tissues by 329 and 300%, respectively. [Conclusion] The results of this investigation clearly showed that omega-3 fatty acids strongly inhibited human breast cancer proliferation both in vitro and in vivo via formation of reactive oxygen species and induction of apoptosis by caspase 8 activation. This study calls for further studies in human subjects to assess the effectiveness of fish oil as a dietary supplement in the treatment of certain types of cancers. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 229.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.