Methylsulfonylmethane decreases inflammatory response to tumor necrosis factor-α in cardiac cells

Am J Cardiovasc Dis. 2018 Jun 15;8(3):31-38. eCollection 2018.


The development of various cardiovascular diseases (CVDs) are associated with chronic inflammation. Tumor necrosis factor α (TNF-α) is a pro-inflammatory cytokine that activates the nuclear factor-κB (NF-κB) signaling pathway, leading to increased inflammatory cytokine expression, such as interleukin-6 (IL-6). Interventions to reduce each of these factors have been demonstrated to reduce the development of CVD. Methylsulfonylmethane (MSM) is a naturally occurring compound that demonstrates anti-inflammatory effects in humans and various animal and cell culture models. The effects of MSM include decreased NF-κB activation, decreased expression of TNF-α, and IL-6. However, the effects of MSM within the heart have not yet been examined. Therefore, the purpose of this investigation was to determine whether MSM protects cardiac cells from inflammation that occurs in response to pro-inflammatory stimuli. A novel immortalized human ventricular cardiomyocyte cell line, designated Ac16, developed and characterized in the laboratory of Dr. Mercy Davidson, Columbia Invention Report No. 823, U.S. patent No. 7,223,599 were utilized. Cells were treated with TNF-α, alone or in combination with MSM. To confirm an appropriate dosage of MSM, the effect of various concentrations on cell viability, and IL-6 production were examined. The effect of MSM on transcript expression of pro-inflammatory markers and activation of NF-κB were examined with the established dose by real-time quantitative PCR and western blot, respectively. MSM treatment combined with TNF-α significantly decreased IL-6 production and transcript expression compared to TNF-α alone. These findings indicate that MSM may protect against inflammation in the heart, and thereby protect against inflammation-linked CVDs. Further study is warranted to determine the effect of MSM on cardiovascular health outcomes.

Keywords: IL-6; MSM; Methylsulfonylmethane; NF-κB; TNF-α; cardiac; inflammation.