Lipid emulsion as a vehicle for propofol
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Dear Editor,
I read with great interest the article, titled ‘Receptor subtype-dependent effects of propofol on metalloproteinase activity, NKG2D ligand expression, and NK cell-mediated cytotoxicity in breast cancer: an in vitro study,’ recently published in the Korean Journal of Anesthesiology [1]. This work presented by Ri et al. [1] represents a valuable contribution to the field, and I commend the authors for their investigation. The authors reported that propofol upregulates both the mRNA and protein levels of the natural killer group 2 member D (NKG2D) ligand in MCF-7 (that expresses estrogen and progesterone receptors) and HCC-70 (a triple-negative subtype) breast cancer cell lines [1]. This enhanced expression increases the susceptibility of these cells to the cytotoxic effects mediated by natural killer cells [1]. In contrast, propofol exposure leads to a reduction in both the transcript and surface presence of the NKG2D ligand in MDA-MB-453 breast cancer cell lines that are characterized by the positive expression of human epidermal growth factor receptor 2 [1]. Initially formulated for use in parenteral nutrition, lipid emulsions are now broadly utilized in the management of systemic toxicity caused by local anesthetics [2]. They have also been shown to mitigate cardiovascular collapse resulting from an overdose of highly lipophilic non-local anesthetic agents in patients that do not respond to conventional supportive therapies [2]. Lipid emulsions also serve as delivery vehicles for anesthetic agents, including propofol and etomidate [2]. In particular, however, I would like to comment on the control group used in this study [1]. The control group received an equivalent volume of distilled water [1], while the 1% propofol solution (Anepol, Hana Pharm Co.) was formulated as a 10% Intralipid emulsion. Given that the administered concentrations of 4 and 8 μg of propofol per 1 ml of culture medium are dissolved in 0.4 μl and 0.8 μl of 10% Intralipid, respectively, it would have been more appropriate to use 0.8 μl of 10% Intralipid per 1 ml of medium as the control, rather than using distilled water of equal volume. This would provide a more accurate comparison by considering the lipid-based vehicles present in the experimental groups. In laboratory settings, commercially formulated propofol can be solubilized using dimethyl sulfoxide (DMSO). Consequently, in comparable studies investigating the effect of propofol on breast cancer cell lines, DMSO has been used as the control vehicle [3]. Intralipid, composed entirely of long-chain fatty acids derived from soybean oil and consisting of approximately 53% linoleic acid, 24% oleic acid, 11% palmitic acid, 8% alpha-linolenic acid, and 4% stearic acid, has been shown to suppress cell viability in Caco-2 colon cancer cells [4,5]. In light of such prior studies, it is essential to assess the effect of 10% Intralipid—at the same volume used to dissolve propofol—on natural killer cell-mediated immune responses in breast cancer cell lines. This approach would help isolate the specific effects of propofol and eliminate the potential confounding influences introduced by the lipid vehicle.
Notes
Funding: None.
Conflicts of Interest: No potential conflict of interest relevant to this article was reported.
This article is a reader’s comment on the original paper "Receptor subtype-dependent effects of propofol on metalloproteinase activity, NKG2D ligand expression, and NK cell-mediated cytotoxicity in breast cancer: an in vitro study."
The authors of the original article were invited to respond to this letter but did not reply. In accordance with our editorial policy, the letter is being published independently to contribute to the ongoing academic discussion.