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. 2025 Feb 28;26(5):2176.
doi: 10.3390/ijms26052176.

Cranberry Oil: A Potent Natural Intimate Care Ingredient Displaying Antioxidant and Anti-Inflammatory Effects and Promoting Beneficial Vaginal Lactobacillus

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Cranberry Oil: A Potent Natural Intimate Care Ingredient Displaying Antioxidant and Anti-Inflammatory Effects and Promoting Beneficial Vaginal Lactobacillus

Cloé Boira et al. Int J Mol Sci. .

Abstract

Cranberry oil is known for nutritional benefits, and this work is aimed at studying its soothing properties and potential as an intimate care ingredient. The antioxidant, anti-inflammatory, and anti-irritation properties of cranberry oil were evaluated on epithelial cells and tissues, including the vaginal epithelium. The impact of the oil on vaginal microbiota was assessed in vitro. Cranberry oil reduced oxidative stress in keratinocytes (ROS -43%) and lowered inflammation by lessening the release of cytokines IL-8 (-33%) and TNF-α (-32%). Irritation induced by sodium dodecyl sulfate (SDS) in skin explants was lowered by 24%. Cranberry oil and fruit extract acted synergistically on inflammation, decreasing TNF-α release by 75% (vs. -34% and -16%, respectively). Cranberry oil reduced inflammation on EpiVaginal™ tissue, decreasing IL-6 by 36%. The minimum inhibitory concentration (MIC) of cranberry oil on the pathogenic vaginal microorganisms C. albicans and G. vaginalis was 0.5% and 0.1%, respectively. The oil promoted the growth of commensal L. jensenii (×79 at 0.1%) and favored a high proportion of lactic acid bacteria when co-cultured with C. albicans. Cranberry oil has antioxidant, anti-inflammatory, and soothing properties on skin. Anti-inflammatory activity was confirmed on vaginal epithelium, and initial in vitro evidence indicates that the oil can balance vaginal flora to prevent dysbiosis.

Keywords: Candida albicans; Gardnerella vaginalis; Lactobacillus; Vaccinium macrocarpon; cranberry; epithelium; fatty acids; intimate care; keratinocytes; skin; vaginal flora.

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Conflict of interest statement

Authors Cloé Boira, Julia Jolibois, Anaïs Durduret, Caroline Szewezyk, Morgane De Tollenaere, Amandine Scandolera, and Romain Reynaud are employed by the company Givaudan Active Beauty. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
ROS (reactive oxygen species) production in normal human epidermal keratinocytes. Oxidative stress was induced with TBP at 5 mM (tert-Butyl hydroperoxide), and keratinocytes were pre-treated with the antioxidant reference molecule, resveratrol at 200 µM (positive control), or with cranberry oil at 0.05%. ROS production is expressed in percentage of TBP-treated condition. Mann–Whitney U-test, * p < 0.05.
Figure 2
Figure 2
Release of (A) cytokines IL-8 (Interleukin 8) and (B) TNF-α (Tumor Necrosis Factor alpha) (B) in normal human epidermal keratinocytes stressed with PMA (Phorbol 12-Myristate 13-Acetate) and pre-treated with the anti-inflammatory reference compound dexamethasone at 1 µM (positive control) or cranberry oil at 0.005%. Quantification of cytokines is expressed as a percentage of the response of PMA treated condition. Mann–Whitney U-test, ** p < 0.01, *** p < 0.001.
Figure 3
Figure 3
Release of cytokine IL-6 (Interleukin 6) EpiVaginal™ tissues stressed with flagellin 100 ng/mL and pre-treated with the anti-inflammatory reference compound dexamethasone at 1 µM (positive control) or cranberry oil at 0.05%. Quantification of IL-6 is expressed as a percentage of the response of flagellin-treated condition. Mann–Whitney U-test, * p < 0.5, ** p < 0.01, *** p < 0.001.
Figure 4
Figure 4
Irritation scoring on skin explants stressed with SDS at 0.2% (sodium dodecyl sulfate). Mann–Whitney U-test, *** p < 0.001, ns not significant.
Figure 5
Figure 5
Morphological aspect of the skin explants: (A) untreated; (B) treated with SDS at 0.2% (sodium dodecyl sulfate) to induce irritation characterized by an altered barrier function, edema, and flat dermal–epidermal junction (DEJ), indicated by arrows; and (C) pre-treated with cranberry oil 0.5% before irritation induction with SDS at 0.2%. Skin explant slices from a 45-year-old woman were treated with hematoxylin and eosin staining for microscopic observation (magnification x10). All images shown are from the same donor.
Figure 6
Figure 6
Growth of Candida albicans (black square) and Gardnerella vaginalis (gray triangle) without cranberry oil and in the presence of a range of concentration of oil from 0.001% to 0.5%, to determine minimum inhibitory concentration. Growth is expressed in percentage of the OD 600 nm of the control culture. Mann–Whitney U-test with * p < 0.05.
Figure 7
Figure 7
Growth of Lactobacillus jensenii based on the OD 600 nm of the culture expressed as a percentage of the control culture without cranberry oil and in the presence of a range of concentrations of the oil, from 0.001% and 0.5% (black dots), and pH of the culture (gray squares). Mann–Whitney U-test with * p < 0.05.
Figure 8
Figure 8
Percentage of Lactobacillus jensenii (gray) and Candida albicans (black) in a co-culture with or without cranberry oil at 0.5% and pH measurements.
Figure 9
Figure 9
Release of TNF-α (Tumor Necrosis Factor alpha) in normal human epidermal keratinocytes stressed with PMA (Phorbol 12-Myristate 13-Acetate) and pre-treated with anti-inflammatory reference compound dexamethasone at 1 µM (positive control), cranberry extract at 0.5 mg/mL, cranberry oil at 0.05% or 0.05%, or with a combination of cranberry extract 0.5 mg/mL and cranberry oil at 0.05% or 0.005%. Quantification of cytokines is expressed as a percentage of the response of PMA-treated condition. Mann–Whitney U-test, # p < 0.1, * p < 0.05, ** p < 0.01, *** p < 0.001.

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