Ultraviolet B-irradiated mushroom supplementation increased the Ca++ uptake and ameliorated the LPS-induced inflammatory responses in zebrafish larvae.

The harmful effects of excessive ultraviolet (UV) exposure are well known. However, moderate exposure to UV radiation is beneficial and required for active vitamin D synthesis in our body. People living in the coldest regions on the earth are unable to expose their skin to the solar UV radiation and, therefore, additional supplementation of Vitamin D2 is recommended. Mushrooms are one such consumable macrofungi, which has high vitamin content and therefore used in various traditional medicines. Particularly, UVB-irradiated mushrooms are rich in active vitamin D content and that is why recommended to include in the daily diets for the patients suffering from the problems associated with bone mineralization. In the present study, we evaluated the cytotoxic effect of mushroom extract (UVB-ME) (Lentinus edodes) treatment against MG-63 cells, HepG2 cells, and CCD 841 CoN cells. Furthermore, we elucidated the potential of UVB-ME on Ca++ uptake in osteoblast-like MG-63 cells. Next, we validated the response of Ca++ uptake on the growth and development of zebrafish larvae. In addition, the anti-inflammatory and immunomodulatory potential of UVB-ME treatment against lipopolysaccharide-induced inflammatory response was also analyzed in vivo. Collectively, the study suggested that dietary supplementation of UVB-irradiated mushroom is beneficial for bone calcification and could modulate the host immune system.

Metasequoia glyptostroboides potentiates anticancer effect against cervical cancer via intrinsic apoptosis pathway.

This study was undertaken to investigate the anticancer effects of organic extracts derived from the floral cones of Metasequoia glyptostroboides. Dried powder of M. glyptostroboides floral cones was subjected to methanol extraction, and the resulting extract was further partitioned by liquid-liquid extraction using the organic solvents n-hexane, dichloromethane (DME), chloroform, and ethyl acetate in addition to deionized water. HeLa cervical and COS-7 cells were used as a cancer cell model and normal cell control, respectively. The anticancer effect was evaluated by using the Cell Counting Kit-8 assay. The viability of COS-7 cells was found to be 12-fold higher than that of the HeLa cells under the administration of 50 µg/ml of the DME extract. Further, the sub-G1 population was determined by FACS analysis. The number of cells at the sub-G1 phase, which indicates apoptotic cells, was increased approximately fourfold upon treatment with the DME and CE extracts compared with that in the negative control. Furthermore, RT-qPCR and western blotting were used to quantitate the relative RNA and protein levels of the cell death pathway components, respectively. Our results suggest that the extracts of M. glyptostroboides floral cones, especially the DME extract, which possesses several anticancer components, as determined by GC-MS analysis, could a potential natural anticancer agent.

Bamboo leave extract ameliorated 12-O-tetradecanoylphorbol-13-acetate (TPA) induced ear inflammation by reducing MAP kinase levels and NF-κB activation in mice model.

Sasa coreana Nakai (SCN) is a medicinal plant commonly used against inflammation. However, the underlined mechanisms against skin inflammation is poorly understood. The present study investigated the effects of SCN leave extract on ear inflammation. To this aim, six-week-old male ICR mice was subjected to 12-O-tetradecanoyl-phorbol-13-acetate induce ear edema, which were then topically treated with the leave extract of SCN. Ear thickness, weight, and morphological changes were recorded to ensure the induction of ear edema. Further, histological analysis and protein expression for inflammatory markers were also recorded to validate the study. Topical treatment with SCN repressed TPA-induced ear edema in a dose-dependent manner. Further, SCN treatment significantly antagonized the protein expression of MAP kinase signaling pathway and reduced the effect of TPA-induced NF-κB activation, sequentially, deactivated its transcriptional targets in a dose-dependent manner. Collectively, the study suggested that SCN could be a useful therapeutic agent against skin inflammation.

Phorbol 12-Myristate 13-Acetate Induced Toxicity Study and the Role of Tangeretin in Abrogating HIF-1α-NF-κB Crosstalk In Vitro and In Vivo.

Phorbol 12-myristate 13-acetate (PMA) is a potent tumor promoter and highly inflammatory in nature. Here, we investigated the toxic effects of PMA on different model system. PMA (10 µg) caused chromosomal aberrations on the Allium cepa root tip and induced mitotic dysfunction. Similarly, PMA caused embryonic and larval deformities and a plummeted survivability rate on zebrafish embryo in a dose-dependent manner. Persistently, PMA treatment on immortalized human keratinocyte human keratinocyte (HaCaT) cells caused massive inflammatory rush at 4 h and a drop in cell survivability at 24 h. Concomitantly, we replicated a cutaneous inflammation similar to human psoriasis induced by PMA. Herein, we used tangeretin (TAN), as an antagonist to counteract the inflammatory response. Results from an in vivo experiment indicated that TAN (10 and 30 mg/kg) significantly inhibited PMA stimulated epidermal hyperplasia and intra-epidermal neutrophilic abscesses. In addition, its treatment effectively neutralized PMA induced elevated reactive oxygen species (ROS) generation on in vitro and in vivo systems, promoting antioxidant response. The association of hypoxia-inducible factor 1-alpha (HIF-1α)-nuclear factor kappa-light-chain-enhancer of activated b cells (NF-κB) crosstalk triggered by PMA enhanced PKCα-ERK1/2-NF-κB pathway; its activation was also significantly counteracted after TAN treatment. Conclusively, we demonstrated TAN inhibited the nuclear translocation of HIF-1α and NF-κB p65. Collectively, TAN treatment ameliorated PMA incited malignant inflammatory response by remodeling the cutaneous microenvironment.

Genotypic, phenotypic, and pathogenic characterization of the soil isolated Acinetobacter courvalinii.

Most of the human gene homologs are found in Caenorhabditis elegans. As a wide variety of micro-organisms present in the environment is pathogens, so, C. elegans could be a useful model to track future infectious disease. With this knowledge, in this study, we isolated Acinetobacter courvalinii from the soil and characterized its pathogenicity for the first time. For the isolation, we used Glucose-Yeast extract-Ethanol-Calcium carbonate medium. To this aim, we evaluated the resistivity of bacteria against several stressful microenvironments. As we observed, A. courvalinii JP_A1001 shown highly tolerance against the acidic environment (pH 3-7), resistant against up to 0.2% of phenol content, and survived in the medium supplemented with 0.3% of bile salt. In addition, the bacteria were also resistant against several antibiotics showing the property of multidrug-resistant bacteria. Moreover, the isolated bacteria have shown the biofilm formation ability within 60 h. Further, we found that incubation of C. elegans with A. courvalinii JP_A1001 decreased the body movement and increased the free radical generation which remarkably influenced the life expectancy of C. elegans compared to E. coli OP50. Therefore, we concluded that A. courvalinii JP_A1001 found in the soil could be a future threat as a pathogen to public health.

Aflatoxin B1 induces reactive oxygen species-dependent caspase-mediated apoptosis in normal human cells, inhibits Allium cepa root cell division, and triggers inflammatory response in zebrafish larvae.

Mycotoxin contamination of food and water is a serious global concern. Aflatoxin B1 (AFB1) is a deadly mycotoxin that contaminates both food and water bodies in the environment. AFB1 is reported to cause severe health issues, including hepatotoxicity, teratogenicity, and immunotoxicity in humans; however, the mechanistic effects on plant and aquatic animals are not fully understood. To obtain a clear understanding of the effects of AFB1 on the ecosystem, we examined the influence of AFB1 exposure on different model systems corresponding to various habitats. In the current study, AFB1 contamination consequences were studied on a human normal cell lines (HaCaT, CCD 841 CoN), meristematic Allium cepa (onion) root cells, and zebrafish embryonic development. Our results clearly indicate that concentrations of AFB1 >10 µM are toxic to HaCaT cells. Morphological changes of HaCaT and CCD 841 CoN cells were clearly observed after exposure to AFB1. Particularly in HaCaT cells, treatment with 50 µM and 100 µM AFB1induces oxidative stress by excessive endogenous free-radical production such as ROS and NO generation. These consequences accelerate the ROS-dependent DNA damage events, which subsequently result in caspase mediated programmed cell death. Exposure of A. cepa root cells to AFB1 for 24 h resulted in abnormal cell division. A. cepa root cells subjected to AFB1 treatment showed a significant concentration-dependent increase in metaphase arrest. Exposure of zebrafish embryos to AFB1 also revealed that AFB1 contamination restricts the larval growth and development, resulting in a remarkably increased zebrafish mortality rate. Collectively, results of the current study indicate that AFB1 contamination triggers the programmed cell death machinery, subsequently affecting the ecosystem.