CONFERENCE PROCEEDING
Treatment of bee venom-induced toxicity with c. polygonoides: A study focusing on inflammation and apoptosis
1
Department of Medical Pharmacology, Faculty of Medicine, Şeyh Edebali University, Bilecik, Türkiye
2
Center of Toxicology Science and Applications, Medical School, University of Crete, Heraklion, Crete, Greece
3
Universidad Ecotec, Samborondón, Ecuador
4
I.M. Sechenov First State Medical University, Moscow, Russia
Publication date: 2026-07-30
Public Health Toxicol 2026;6(Supplement 1):A26
KEYWORDS
ABSTRACT
Introduction:
Bee venom contains compounds such as adrenaline, dopamine, histamine, mellitin, phospholipases A2 (PLA2s), phospholipases B, and serotonin. Melittin is the main and most toxic compound in bee venom, comprising 50–60% of the total venom. Melittin causes allergic reactions and pain caused by bee stings. Accumulated melittin and PLA2 act synergistically with lipid membranes, leading to cell damage. Currently, various therapeutic methods are used for the treatment of bee venom-induced toxicity. C. polygonoides Linn. belongs to the Polygonaceae family and does not require any vegetation for growth. C. polygonoides (CP) flowers contain high amounts of protein and have digestive properties. Based on this information in the literature, our study aimed to determine the effects of CP on bee venom toxicity.
Methods:
A linear wound model was studied on the fibroblast cell line (L929), and each cell group was treated with 5 µg/ml bee venom. CP doses of 1, 2.5, and 5 µg/ml were used for treatment. After treatment, cells were incubated for 48 hours, and semi-quantitative analyses of MTT, LDH, TAC, TOS, and PPAR-γ, as well as Annexin V+PI+DAPI expression, were performed using immunofluorescence staining. The findings were statistically evaluated to determine their significance.
Results:
When the results were examined, bee venom (5 µg/ml) induced a significant apoptotic effect on L929 cells. Cell viability decreased by 44.58%, and the level of oxidative damage increased significantly (P<0.01). Following CP treatment, antioxidant and anti-apoptotic effects against bee venom occurred with increasing doses. In particular, the CP 5 µg/ml dose increased cell viability approximately 1.75-fold compared to the bee venom group (P<0.01), bringing it closer to the control group. Similarly, it increased PPAR-γ activation 3.2-fold, maintaining mitochondrial stability and increasing TAC levels. Contrary to PPAR-γ and TAC levels, decreased TOS and LDH levels were observed. Immunofluorescence findings indicate a decrease in Annexin (FITC)/PI antibody levels, which inhibits apoptosis.
Conclusion:
This study demonstrated that C. polygonoides promotes proliferation by reducing apoptosis and inflammation in bee venom-induced toxicities. This therapeutic effect contributes to the literature for future studies.
Bee venom contains compounds such as adrenaline, dopamine, histamine, mellitin, phospholipases A2 (PLA2s), phospholipases B, and serotonin. Melittin is the main and most toxic compound in bee venom, comprising 50–60% of the total venom. Melittin causes allergic reactions and pain caused by bee stings. Accumulated melittin and PLA2 act synergistically with lipid membranes, leading to cell damage. Currently, various therapeutic methods are used for the treatment of bee venom-induced toxicity. C. polygonoides Linn. belongs to the Polygonaceae family and does not require any vegetation for growth. C. polygonoides (CP) flowers contain high amounts of protein and have digestive properties. Based on this information in the literature, our study aimed to determine the effects of CP on bee venom toxicity.
Methods:
A linear wound model was studied on the fibroblast cell line (L929), and each cell group was treated with 5 µg/ml bee venom. CP doses of 1, 2.5, and 5 µg/ml were used for treatment. After treatment, cells were incubated for 48 hours, and semi-quantitative analyses of MTT, LDH, TAC, TOS, and PPAR-γ, as well as Annexin V+PI+DAPI expression, were performed using immunofluorescence staining. The findings were statistically evaluated to determine their significance.
Results:
When the results were examined, bee venom (5 µg/ml) induced a significant apoptotic effect on L929 cells. Cell viability decreased by 44.58%, and the level of oxidative damage increased significantly (P<0.01). Following CP treatment, antioxidant and anti-apoptotic effects against bee venom occurred with increasing doses. In particular, the CP 5 µg/ml dose increased cell viability approximately 1.75-fold compared to the bee venom group (P<0.01), bringing it closer to the control group. Similarly, it increased PPAR-γ activation 3.2-fold, maintaining mitochondrial stability and increasing TAC levels. Contrary to PPAR-γ and TAC levels, decreased TOS and LDH levels were observed. Immunofluorescence findings indicate a decrease in Annexin (FITC)/PI antibody levels, which inhibits apoptosis.
Conclusion:
This study demonstrated that C. polygonoides promotes proliferation by reducing apoptosis and inflammation in bee venom-induced toxicities. This therapeutic effect contributes to the literature for future studies.
CONFLICTS OF INTEREST
The authors declare that they have no conflicts of interest in the publication of this article. The authors have no conflicts of interest to report in this work. Abstract was not submitted elsewhere and is first published here.
FUNDING
The project was partially funded by the European Union's "Horizon Europe" framework programme, project name: "European Partnership for the Assessment of Risks from Chemicals (PARC)".
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| eISSN: | 2732-8929 |
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