Cell death in the midgut epithelium of the worker honey bee (Apis mellifem carnica) during metamorphosis

1980 ◽  
Vol 94 (2) ◽  
pp. 217-224 ◽  
Author(s):  
Nada Pipan ◽  
Vida Rakovec

2017 ◽  
Author(s):  
Faranak Shiassi Arani ◽  
Latifeh Karimzadeh ◽  
Seyed Mohammad Ghafoori ◽  
Mohammad Nabiuni

ABSTRACTHoney Bee Venom has various biological activities such as inhibitory effect on several types of cancer. Cisplatin is an old and potent drug to treat the most of cancer. Our aims in this study were determination of the anti-mutagenic and cytotoxic effects of HBV on mammary carcinoma, lonely and in combination with cisplatin. In this study 4T1 cell line were cultured and incubated at 37 C in humidified CO2-incubator. The cell viabilities were examined by MTT assay. Also HBV was screened for its anti-mutagenic activity against sodium azide by Ames test. The result showed that 6μg/ml HBV, 20μg/ml cisplatin and 6μg/ml HBV with 10μg/ml cisplatin can induce an approximately 50% 4T1 cell death. 7mg/ml HBV with the inhibition of 62.76% sodium azide showed high potential in decreasing the mutagenic agents. MTT assay demonstrated that HBV and cisplatin can cause cell death in a dose-dependent manner. The cytotoxic effect of cisplatin is also promoted by HBV. Ames test results indicated that HBV can inhibit sodium azide as a mutagenic agent. Anti-mutagenic activity of HBV was increased significantly in presence of S9 mix. Hence, our findings reveal that HBV can enhance the cytotoxic effect of cisplatin drug and it has cancer preventing effects.



2015 ◽  
Vol 81 ◽  
pp. 36-41 ◽  
Author(s):  
Isobel Ronai ◽  
Deborah A. Barton ◽  
Benjamin P. Oldroyd ◽  
Vanina Vergoz




2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Faranak Shiassi Arani ◽  
Latifeh Karimzadeh ◽  
Seyed Mohammad Ghafoori ◽  
Mohammad Nabiuni

Introduction. Honey bee venom (HBV) has various biological activities such as the inhibitory effect on several types of cancer. Cisplatin is an old and potent drug to treat most of the cancers. Our aim in the present study was to determine antimutagenic and cytotoxic effects of HBV on mammary carcinoma, exclusively and in combination with cisplatin. Methods. In this study, 4T1 cell line was cultured in RPMI-1640 with 10% fetal bovine serum (FBS), at 37°C in humidified CO2 incubator. The cell viabilities were examined by the MTT assay. Also, HBV was screened‏ for its antimutagenic activity via the Ames test. The results were assessed by SPSS software version 19 and one-way ANOVA method considering p<0.05 level of significance. Results. The results showed that 6 mg/ml of HBV, 20 μg/ml of cisplatin, and 6 mg/ml HBV with 10 μg/ml cisplatin could induce approximately 50% of 4T1 cell death. The concentration 7 mg/ml of HBV with of 62.76% inhibitory rate showed the highest antimutagenic activity in comparison with other treatment groups. Conclusions. The MTT assay demonstrated that HBV and cisplatin could cause cell death in a dose-dependent manner. The cytotoxic effect of cisplatin also promoted by HBV. Ames test outcomes indicated that HBV could act as a significant mutagenic agent. The antimutagenic activity of HBV was increased considerably in the presence of S9 mix. Therefore, our findings have revealed that HBV can enhance the cytotoxic effect of cisplatin drug and its cancer-preventing effects.





2015 ◽  
Vol 108 (4) ◽  
pp. 1486-1494 ◽  
Author(s):  
Yan-Yan Wu ◽  
Ting Zhou ◽  
Qiang Wang ◽  
Ping-Li Dai ◽  
Shu-Fa Xu ◽  
...  


2016 ◽  
Vol 25 (5) ◽  
pp. 646-652 ◽  
Author(s):  
I. Ronai ◽  
B. P. Oldroyd ◽  
V. Vergoz


Antibiotics ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 517
Author(s):  
Sirikwan Sangboonruang ◽  
Kuntida Kitidee ◽  
Panuwan Chantawannakul ◽  
Khajornsak Tragoolpua ◽  
Yingmanee Tragoolpua

Melittin, a major component found in bee venom, is produced by the Apis species of the honey bee. In this study, the effect of melittin derived from Apis florea (Mel-AF), which is a wild honey bee species that is indigenous to Thailand, was investigated against human malignant melanoma (A375) cells. In this study, Mel-AF exhibited considerable potential in the anti-proliferative action of A375 cells. Subsequently, the cellular mechanism of Mel-AF that induced cell death was investigated in terms of apoptosis. As a result, gene and protein expression levels, which indicated the activation of cytochrome-c release and caspase-9 expression, eventually triggered the release of the caspase-3 executioner upon Mel-AF. We then determined that apoptosis-mediated cell death was carried out through the intrinsic mitochondrial pathway. Moreover, advanced abilities, including cell motility and invasion, were significantly suppressed. Mel-AF manipulated the actin arrangement via the trapping of stress fibers that were found underneath the membrane, which resulted in the defective actin cytoskeleton organization. Consequently, the expression of EGFR, a binding protein to F-actin, was also found to be suppressed. This outcome strongly supports the effects of Mel-AF in the inhibition of progressive malignant activity through the disruption of actin cytoskeleton-EGFR interaction and the EGFR signaling system. Thus, the findings of our current study indicate the potential usefulness of Mel-AF in cancer treatments as an apoptosis inducer and a potential actin-targeting agent.



2010 ◽  
Vol 42 (1) ◽  
pp. 24-31 ◽  
Author(s):  
M.M. Rost-Roszkowska ◽  
R. Machida ◽  
M. Fukui
Keyword(s):  


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