From Gyeongsang National University:
Aged Red Garlic Extract Reduces Cigarette Smoke Extract-induced Cell Death in Human Bronchial Smooth Muscle Cells by Increasing Intracellular Glutathione Levels
Yi-Yeong Jeong, Hye-Jin Park, Young-Woo Cho, Eun-Jin Kim, Gyu-Tae Kim, Yun-Ja Mun, Jong Deog Lee, Jung-Hye Shin, Nak-Ju Sung, Dawon Kang, Jaehee Han
[Ed.] Phytother. Res., Jan 2012; 26: 18–25.
Article first published online: 28 APR 2011. DOI: 10.1002/ptr.3502
... A fluorochrome inhibitor of caspase (FLICA) apoptosis detection kit was used to detect active caspases (Immunochemistry Technologies, Bloomington, MN, USA). ... In the CSE-treated cells, the apoptotic cells that were stained by FLICA were significantly increased compared with the control (Fig. 1B)...
Abstract:
Increasing antioxidant capacity has been proposed as a promising strategy to prevent cigarette smoke-induced lung diseases. This study tested whether garlic extracts prevented cigarette smoke extract (CSE)-induced cell death in human bronchial smooth muscle cells (HBSMCs). Garlic extracts were prepared from fresh raw garlic (FRG), aged black garlic (ABG) and aged red garlic (ARG). Treatment of HBSMCs with 10% CSE induced cell death accompanied by activation of caspase. Of the garlic extracts, treatment with ARG extract reduced CSE-induced cell death. The combination of ARG extract with CSE attenuated the CSE-induced reduction in glutathione (GSH) content, generation of reactive oxygen species (ROS) and induction of heme oxygenase-1 expression compared with CSE treatment without ARG extract. Furthermore, the combination of L-BSO, a GSH synthesis inhibitor, with ARG and CSE extracts failed to increase the intracellular GSH content and cell viability. Taken together, these results demonstrate that ARG extract reduces CSE-induced cell death by increasing GSH content and reducing ROS generation in HBSMCs.
Keywords: smoking; garlic; glutathione; reactive oxygen species; smooth muscle; bronchiole
Copyright © 2011 John Wiley & Sons, Ltd.
From Korea University, Korea University College of Medicine, Rice University (TX, USA):
Antitumor therapeutic effects of a genetically engineered Salmonella typhimurium harboring TNF-α in mice.
Yoon, Won Suck, Yang Seok Chae, Juyeon Hong, and Yong Keun Park
Applied microbiology and biotechnology, Mar 2011; 89(6), 1807-1819.
... natural killer (NK) cells on C57BL/6 background were contributed by CW Hong, SH Park (Korea University, Korea). ... with different microbe for 24 h. After 24 h, the cells were stained with FLICA Apoptosis detection kit caspase assay (Immunochemistry Technologies, LLC ...
Abstract:
Although the use of TNF-α in the treatment of cancer is restricted due to its non-specific cytotoxicity and narrow range of applications to different cancers in clinical trials, we investigated a safe anti-cancer drug by the use of engineered bacterial capsule harboring TNF-α. The engineered bacterial capsule was designed to target cancer cells, promote a tumor-suppressive environment, and increase the efficacy of existing cancer treatments, including chemotherapy, radiotherapy, and cell therapy. The engineered bacterial capsule was constructed with Salmonella capsulizing TNF-α protein, which was produced and capsulized by Salmonella to reduce side effects of the protein. This bacterial capsule induced a tumor-suppressive environment through the activation of natural killer cells. Engineered bacterial capsule invaded tumor cells, released TNF-α, and induced apoptosis of tumor cells without apparent side effects. In a murine melanoma model, the bacterial capsule of TNF-α significantly inhibited tumor growth by 80–100% and prolonged the survival of the mice. When tested in combination with chemotherapy (cisplatin), antibiotics, and vaccine, recombinant microbial treatment increased the anti-tumor effects of existing therapies. The anti-tumor effects of the bacterial capsule of TNF-α were also observed in cervical cancer, melanoma, breast cancer, colon cancer, and renal carcinoma. These results suggest that the bacterial capsule of TNF-α is a promising strategy for TNF-α treatment.
Keywords: Antitumor effects, tumor treatments, TNF-a, Salmonella typhimurium
From Kyung Hee University School of Medicine, Wonkwang University, Yonsei University, and CSI/BS Metropolitan Agency:
Effects of Fraction obtained from Korean Corni Fructus extracts causing anti-proliferation and p53-dependent apoptosis in A549 lung cancer cells.
Choi, Won-Hyung, Jong-Phil Chu, Mei-Hua Jiang, Seung-Hwa Baek, and Hyun-do Park
Nutrition and cancer, 2011; 63(1), 121-129.
Published online: 04 Dec 2010. DOI: 10.1080/01635581.2010.516475
... The caspase-3 (FLICA FAM-DEVD-FMK), caspase-8 (FLICA FAM-LETD-FMK), and caspase-9 kits (FLICA FAM-LEHD-FMK) were purchased from Immunochemistry Technologies,LLC (Bloomington ... A549 cells were labeled with FAM-DEVD-FMK (caspase-3 ...
Abstract:
Corni Fructus has traditionally been used as herbal medicine for the treatment of tuberculosis, asthma, hepatitis, and chronic nephritis in Korea, Japan, and China. This research was carried out to evaluate the proliferative-inhibitory effect of CF extracts against cancer cells and to identify the new pro-substance from medicinal plants. Among these herbal extracts extracted from KCF (Korean Corni Fructus), JCF (Japanese Corni Fructus) and CCF (Chinese Corni Fructus), KCF extracts strongly induced anti-proliferation of cancer cells in a dose-dependent manner compared with other extracts. Moreover, after treatment with CM/F3 (fraction 3 obtained from KCF extracts) for 24 h, A549 cells were evaluated by several indicators such as cell viability, LDH release, DNA fragmentation, nuclear condensation, and apoptotic proteins in vitro. CM/F3 showed the tumor-selective growth inhibitory activity in a dose- and time-dependent manner in A549 cells. Consistently, CM/F3 effectively induced the activation of bax, cytochrome-c, caspase-3, -8, -9, p53, and p21 causing apoptosis, and caused the suppression of Cdk2, pRb, and E2F1 related to cell arrest in A549 cells. These results demonstrate that CM/F3 caused not only anti-proliferation but also cell death involving cell arrest through interaction between apoptotic proteins and the upregulation of p53 in A549 cells.
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