SkinCeuticals Phloretin CF Serum

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NOTE: The colours indicate the effectiveness of an ingredient. It is ILLEGAL to put toxic and harmful ingredients in skincare products. The crosstalk between AMPK, Nrf2, and SIRT1 pathways in the anti-inflammatory effect of phloretin. The activation of AMPK and SIRT1 are closely related in the regulation of metabolism and pathologies such as oxidative stress and inflammation. Activation of AMPK by phloretin via its phosphorylation as well as increased expression of SERT1 have been associated with its anti-inflammatory effect and modulation of lipid metabolism such as inhibition of lipid accumulation. This activity was further shown to be related to the induction of Nrf2 that suppresses both the oxidative stress and inflammatory pathways induced by a variety of agents including LPS. Increased SERT3 activity by phloretin is also reported. The red line shows the inhibitory response. This study confirms the protective role of a unique mixture of antioxidants containing vitamin C, ferulic acid, and phloretin on human skin from the harmful effects of UV irradiation. Phloretin, in addition to being a potent antioxidant, may stabilize and increase the skin availability of topically applied vitamin C and ferulic acid. We propose that antioxidant mixture will complement and synergize with sunscreens in providing photoprotection for human skin.” The experts from SkinCeuticals are here to help you decide which bestselling antioxidant serum is right for you and what products you should be pairing with it. The other major pathway of the anti-inflmmmatory mechanism for phloretin is the activation of the Nrf2 transcription pathway. This common mechanism of anti-inflammatory and antioxidant response in various cells appears to be shared by many cytoprotective agents. In many experiments, the Nrf2/ARE/HO-1 axis is extensively explored as with modulation by phloretin discussed in this communication under the various sections [ 33, 70, 78, 94, 100, 101, 120]. The Nrf2 signalling has also been shown to be relevant in the anti-inflammatory effect of phlorein in non-immunological cell types. For example, in LPS-stimulated retinal pigment epithelial cells (ARPE-19 cell line), phloretin was shown to suppress the release of proinflammatory cytokines (IL-6, IL-8, and VEGF) through a mechanism associated with an increased level of Nrf2 expression [ 120].

Pure vitamin C (l-ascorbic acid): lauded for its superior antioxidant benefits, this highly potent form of pure vitamin C neutralizes damaging free radicals and protects against oxidative stress while providing visible anti-aging benefits. Delays the deposition of sugar deposits in your skin (sugar hardens collagen, resulting in wrinkles). The effect of phloretin on LPS-induced stimulation of macrophages could be a result of a direct effect on TLRs. Kim et al. [ 49] assessed TLR2/1 heterodimerization and signalling in RAW 264.7 cells by using a selective agonist, Pam 3CSK 4. They have shown that phloretin displays molecular interactions with TLR2/1 and modulates the TLR2 signalling pathway leading to suppressed NF-κB phosphorylation and TNF-α production. Cheon et al. [ 50] used the Propionibacterium acnes-induced skin infection model to examine the effect of phloretin on the TLR-2-mediated inflammatory signalling in human keratinocytes. By measuring secreted embryonic alkaline phosphatase (SEAP) activity induced by either Pam 3CSK 4 or by P. acnes in HEK-Blue TM-hTLR2 cells, which are designed for studying the stimulation of TLR-2 via activation of NF-κB, they were able to confirm the signalling pathway associated with the inhibitory effect of phloretin (5–50 µM). In a similar manor, the P. acnes-stimulated levels of TNF-α, IL-1β, and IL-12 as well as phosphorylated c-Jun N-terminal kinase (JNK) in HaCaT cells was inhibited by phloretin through inhibition of the TLR-2 signalling pathway. While the study by Chang et al. [ 36] (see above) demonstrated phlorizin displays weak or no effect when applied directly on LPS-stimulated RAW 264.7 macrophage, positive results were reported for phlorizin metabolites. When tested at low concentrations (1–5 μg/mL), phloretin 4- O-β-D-glucuronide, 6-methoxyl-phloretin-2- O-β-D-glucuronide, and phloretin-2- O-β-D-glucuronide inhibited NO production and iNOS protein expression [ 51]. Their effect on cytokine expression could however vary and hence a more comprehensive in vivo analysis is needed to assess the potential of phlorizin metabolites as anti-inflammatory agents. In a diabetic neuropathy study induced by STZ, phloretin (50 or 25 mg/kg, i.p.) or in combination with duloxetine (15 mg/kg duloxetine and 25 mg/kg phloretin, i.p.) was shown to ameliorate the thermally induced hyperalgesia, sciatic nerve oxidative stress markers (tissue MDA, NO, SOD activity and GSH levels); and sciatic nerve TNF-α and IL-6 levels [ 107]. This, together with the normalization of histopathological and structural changes, suggests the potential of phloretin as a neuroprotective agent. In HFD- and STZ-induced diabetes models in mice, phlorizin (10–20 mg/kg, p.o.) was shown to alleviate depression symptoms, reversed the decline in GSH, BDNF, and its receptor (TrkB), cyclic AMP-responsive element-binding protein (CREB) and ERK level [ 108]. Inflammatory markers were not, however, assessed in this study.One common link to the release of the above-mentioned proinflammatory mediators from activated macrophages is the nuclear transcription factor κ-B (NF-κB) which regulates the expression of several genes (e.g., chemokines, cytokines, and adhesion molecules) involved in inflammation. For details of NF-κB signalling, readers can refer to the numerous review articles in the field (e.g., [ 40, 41]). The NF-κB represents a family of protein transcription factors such as NF-κB1 (also named p50), NF-κB2 (also named p52), RelA (also named p65), RelB, and c-Rel. The expression of target genes happens when these transcription factors translocate from the cytoplasm to the nucleus and bind (through their transcriptional transactivation domain at their C-terminus) to the κB enhancer region of the DNA. Since the NF-κB proteins are sequestered in the cytoplasm by binding to inhibitory proteins, including inhibitors of κB (IκB) family members (most important is IκBα, others include IκBβ, IκBε, and their precursors), releasing the NF-κB from the complex is a key cell signalling step in inflammatory genes activation. Many agents that activate the inflammatory pathway such as LPS stimulate the degradation of IκBα via the multi-subunit IκB kinase (IKK)-induced phosphorylation. This further triggers ubiquitin-dependent IκBα degradation in the proteasome, thereby allowing the nuclear translocation of NF-κB. The IKK itself is a complex of two kinases (IKKα and IKKβ) and other proteins and constitutes the classic example of the canonical NF-κB pathway of activation which is common to various immunostimulant-based macrophage activation: i.e., the IκBα degradation-execute the canonical activation pathway of NF-κB. A variety of inflammatory stimuli activate the canonical pathway in macrophages, and these include proinflammatory cytokines, pattern-associated molecular patterns (PAMPs), or damage-associated molecular patterns (DAMPs) binding to cognate receptors. The LPS is recognised in macrophages by Toll-like receptors (e.g., TLR4) and its stimulatory effect is orchestrated through the canonical pathway. Other pathways or the noncanonical NF-κB pathway of activation are, however, also known. Activation of macrophages to a phenotypically M1 state leads to the induction of inflammatory mediators (e.g., IL-1, IL-6, IL-12, TNF-α, and chemokines) which promotes the process of inflammation while the M2 phenotype leads to the production of anti-inflammatory cytokines (e.g., IL-10 and IL-13) which promote resolution of inflammation (e.g., during the wound healing stage) [ 42]. Most of the anti-inflammatory mechanisms of phloretin discussed in the following sections are associated with modulation of the above-mentioned signalling pathway of NF-κB including macrophage polarisation. A final way that ascorbic acid can improve the appearance of your skin is through its ability to reduce the appearance of dark spots and correct uneven skin tone. This is accomplished through inhibition of melanin synthesis. Melanin is a pigment that gives our skin color, but too much of this pigment can lead to undesirable dark spots called hyperpigmentation. Ascorbic acid decreases melanin formation by inhibiting tyrosinase, an enzyme that is required for melanin synthesis. Thus, SkinCeuticals Phloretin CF can help the skin to appear brighter with less dark spots and a more even skin tone. The 1-methyl-4-phenyl-1,2,3,6-tetrahydro pyridine (MPTP)-induced Parkinson’s disease (PD) model in mice was employed to explore the neuroprotective effect of phloretin [ 103]. Beyond improving the behavioural symptoms of PD and striatal dopamine level, the increased expression of TNF-α, IL-1β, and IL-6 in brain tissues were suppressed by phloretin treatment (5 mg/kg, p.o.). Moreover, microglial and astrocytes markers expression (glial fibrillary acidic protein, allograft inflammatory factor 1 (Iba-1), iNOS, and COX2), which were increased by MPTP, were also suppressed by phloretin. Given the small dose used in this study, phloretin can be considered a potent inhibitor of neuroinflammation under PD conditions. In the D-GalN-induced aging model of mice, the neuroprotective effect of phlorizin (20 and 40 mg/kg, p.o.) was shown by improvement in memory functions and reversal of histopathological alterations and biochemical parameters of oxidative stress (MDA content and SOD and CAT activities in the serum, liver, and brain) and inflammatory markers (NF-κB activation and IL-1β expression in brain tissues) [ 104]. Correlation between these changes and microbiota alterations as well as restoration also suggests the microbiota-brain axis of neuroprotection. It would be interesting to know whether phloretin could also show similar effects in this experimental model. In the LPS-induced cognitive impairment in mice, phlorizin (10–20 mg/kg, oral) also restored memory functions along with reversing the decreased level of antioxidants (SOD and GSH), the brain-derived neurotropic factor (BDNF) and cholinergic transmission (increased acetylcholinesterase (AChE)) in the hippocampus and cortex [ 105]. On the other hand, phlorizin reversed the increased levels of inflammatory/oxidative markers (TNF-α, IL-6, and MDA). In a sporadic rat model of Alzheimer’s disease induced by injection of Aβ 25–35, phloretin has been shown to improve the spatial memory formation and retention and antioxidant markers as well as the level of TNF-α in the brain homogenates [ 106]. According to a 2008 study, it gives similar results to the classic combo of Vitamin C + Vitamin E + Ferulic Acid:

Text, Behind the formula. Phloretin CF. A bottle of SkinCeuticals Phloretin CF appears as a model turns to us. Icons representing free radicals appear. Text, Pollution, Blue Light, Chemicals, U V. Pure vitamin C (l-ascorbic acid): Lauded for its superior antioxidant benefits, this highly potent form of pure vitamin C neutralizes damaging free radicals and protects against oxidative stress while providing visible anti-aging benefits Another way that ascorbic acid helps to reduce signs of aging is through collagen synthesis. Specifically, ascorbic acid serves as a cofactor for prolysyl and lysyl hydroxylase, the enzymes that are responsible for stabilizing and cross-linking the collagen molecules. Thus, SkinCeuticals Phloretin CF may be able to help reduce the appearance of fine lines and wrinkles while promoting firmer, more youthful skin. Decreases the mRNA level of IL-1β and TNF-α; inhibits the protein and mRNA upregulation of GLUT1 (but not GLUT3 and GLUT4) induced by LPS; inhibits glycolysis in LPS-treated macrophages in a GLUT1-dependent manner.Reduces NO, ROS, TNF-α, and IL-6 production; downregulates the expression of E. coli-induced COX-2, NF-κB pathway, and HO-1 in a concentration-dependent manner. Phloretin CF provides powerful antioxidant protection, suitable for Normal, Oily and Combination skin types to improve discolouration, fine lines and wrinkles with its blend of phloretin, vitamin C and ferulic acid. Green: It’s effective, proven to work, and helps the product do the best possible job for your skin. Prevent, SkinCeuticals, cosmeceutical, Vitamin C, protect, protection, free radicals, Phloretin, stronger skin, youthful skin, radiant skin, natural, normal skin, oily skin, firmer skin The serum comes in a dark bottle with a dropper applicator. The dark colour keeps the actives inside (especially sun sensitive Vitamin C) safe from UV rays that would degrade it and compromise its effectiveness.

SkinCeuticals Phloretin CF is an advanced daytime antioxidant serum that provides superior environmental protection that is a pigment regulator helping to reduce dullness and discolouration of the skin, it retextures and evens skin tone for a brighter more radiant complexion. Suitable for normal, combination skin with ageing and hyperpigmentation. This broad-spectrum treatment provides advanced environmental protection to defend skin against the reactive molecules (including free radicals) that are known to cause cellular damage. In addition to its superior antioxidant capabilities, it has been proven to correct existing damage from the inside out. Having said this, everyone’s skin is different. If your skin is particularly sensitive to alcohol denat and doesn’t tolerate it well,this serum isn’t for you. KEY INGREDIENTS & BENEFITS: Alpha Tocopherol (neutralizes free radicals and replenishes skin lipids), Ferulic Acid (neutralizes free radicals and enhances the antioxidant benefits of vitamins C and E) SkinCeuticals' Phloretin CF provides powerful antioxidant protection to normal, oily and combination skin types. Designed for daytime use, this antioxidant serum neutralizes free radicals to prevent signs of accelerated skin aging. The blend of phloretin, pure vitamin C and Ferulic acid improve the appearance of discoloration, fine lines and uneven skin tone. Phloretin neutralizes damaging free radicals, improves cell turnover and lightens signs of discoloration. L-ascorbic acid protects your skin from oxidative stress while providing visible anti-aging benefits, while ferulic acid enhances the antioxidant benefits of phloretin and vitamin C.

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While C E Ferulic is the ideal topical antioxidant for fine lines, wrinkles, loss of firmness and skin brightening in normal, dry and sensitive skin types, Phloretin CF may be a better choice for normal, oily and combination skin experiencing discoloration along with visible signs of aging. Both topical antioxidants feature L-ascorbic acid (the purest form of vitamin C) and ferulic acid, but the addition of phloretin is what makes Phloretin CF unique. Related: The Truth About Alcohol-Free Skincare: What Does It Really Mean? (Hint: It’s Not What You Think) CE Ferulic is more hydrating, so it’s a better option for dry skin. It also has a less drying delivery system that makes it more suitable for sensitive skin types. Plus, the combination of Vitamin C + Vitamin E + ferulic acid has been around longer and is more studied than the combination of Vitamin C + Ferulic acid + Phloretin, so I’m more inclined to recommend the former. Three-Time Allure Best of Beauty Award Winner: Best Breakthrough, Best Serum, Best Antioxidant Anti-Ager. Elle, Shape, Vogue, InStyle, New Beauty, People. Provides advanced environmental protection from skin-damaging free radicals caused by sun and pollution