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Effect of bee venom on transforming growth factor-beta1-treated hepatocytes.
Int J Toxicol 2010 Jan-Feb; 29(1):49-56IJ

Abstract

Bee venom (BV) has been used as treatment against a wide variety of ailments, including inflammatory diseases. Various studies have demonstrated anti-inflammatory and anticancer effects of BV. Transforming growth factor (TGF)-beta1 induces hepatocyte apoptosis via the mitochondrial permeability transition. However, there is no evidence or information regarding the antiapoptotic effect of BV on hepatocytes. The authors investigated the antiapoptotic effect of BV on TGF-beta1-treated hepatocytes. The results showed significant protection from DNA damage by BV treatment compared to corresponding TGF-beta1-treated hepatocytes without BV. BV suppressed TGF-beta1-induced activation of the bcl-2 family and caspase family of proteins, which resulted in inhibition of poly ADP-ribose polymerase (PARP) cleavage. Furthermore, BV is not cytotoxic in the low concentrations used in this study. Low concentrations of BV potently suppress the apoptotic response in TGF-beta1-treated hepatocytes; therefore, BV may have therapeutic potential for the treatment of liver diseases.

Authors+Show Affiliations

Department of Rehabilitation Medicine, Eulji University Hospital, Daejeon, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20075187

Citation

Park, Jung-Hyun, et al. "Effect of Bee Venom On Transforming Growth Factor-beta1-treated Hepatocytes." International Journal of Toxicology, vol. 29, no. 1, 2010, pp. 49-56.
Park JH, Kim KH, Kim SJ, et al. Effect of bee venom on transforming growth factor-beta1-treated hepatocytes. Int J Toxicol. 2010;29(1):49-56.
Park, J. H., Kim, K. H., Kim, S. J., Lee, W. R., Lee, K. G., Park, J. H., & Park, K. K. (2010). Effect of bee venom on transforming growth factor-beta1-treated hepatocytes. International Journal of Toxicology, 29(1), pp. 49-56. doi:10.1177/1091581809353948.
Park JH, et al. Effect of Bee Venom On Transforming Growth Factor-beta1-treated Hepatocytes. Int J Toxicol. 2010;29(1):49-56. PubMed PMID: 20075187.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of bee venom on transforming growth factor-beta1-treated hepatocytes. AU - Park,Jung-Hyun, AU - Kim,Kyung-Hyun, AU - Kim,Soo-Jung, AU - Lee,Woo-Ram, AU - Lee,Kwang-Gill, AU - Park,Ji-Hyun, AU - Park,Kwan-Kyu, PY - 2010/1/16/entrez PY - 2010/1/16/pubmed PY - 2010/3/24/medline SP - 49 EP - 56 JF - International journal of toxicology JO - Int. J. Toxicol. VL - 29 IS - 1 N2 - Bee venom (BV) has been used as treatment against a wide variety of ailments, including inflammatory diseases. Various studies have demonstrated anti-inflammatory and anticancer effects of BV. Transforming growth factor (TGF)-beta1 induces hepatocyte apoptosis via the mitochondrial permeability transition. However, there is no evidence or information regarding the antiapoptotic effect of BV on hepatocytes. The authors investigated the antiapoptotic effect of BV on TGF-beta1-treated hepatocytes. The results showed significant protection from DNA damage by BV treatment compared to corresponding TGF-beta1-treated hepatocytes without BV. BV suppressed TGF-beta1-induced activation of the bcl-2 family and caspase family of proteins, which resulted in inhibition of poly ADP-ribose polymerase (PARP) cleavage. Furthermore, BV is not cytotoxic in the low concentrations used in this study. Low concentrations of BV potently suppress the apoptotic response in TGF-beta1-treated hepatocytes; therefore, BV may have therapeutic potential for the treatment of liver diseases. SN - 1092-874X UR - https://www.unboundmedicine.com/medline/citation/20075187/Effect_of_bee_venom_on_transforming_growth_factor_beta1_treated_hepatocytes_ L2 - http://journals.sagepub.com/doi/full/10.1177/1091581809353948?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -