SkinCeuticals Phloretin CF Serum

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Instead, you have to trust the science here. Vitamin C + Phloretin + Ferulic Acid can protect your skin from environmental damage so that it ages slowly – but it takes years to see results. 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. Phloretin is a flavonoid found in apples with powerful antioxidant properties. It slow down aging in several ways: The anti-inflammatory potential of phloretin was assessed both in vitro and in vivo using an experimental model of airway inflammation induced by cigarette smoke [ 82]. When the human lung mucoepidermoid cells (NCI-H292 cell line) were exposed to cigarette smoke extract (CSE), the expression of mucin 5ac (MUC5AC) and IL-1β were greatly enhanced, and phloretin suppressed this induction in a dose-dependent manner (1–5 µM). The CSE-induced phosphorylation of epidermal growth factor receptor (EGFR), ERK, and P38 was also inhibited by phloretin. In mice treated with phloretin (10 or 20 mg/kg, i.p.), the effect of CSE in lung histological changes, mucus hypersecretion, MUC5AC expression level, inflammatory cell infiltration in the lungs, and phosphorylation of EGFR, ERK, and P38 were suppressed. Respiratory pathogens ( Haemophilus influenzae) induced chronic obstructive pulmonary disease (COPD) in mice could also be suppressed by phloretin (0.157% in a diet for a week) as evidenced by reduced bacterial burden, inflammatory score in the lungs, and expression of a neutrophil chemoattractant, chemokine (C-X-C motif) ligand 1 (CXCL1) [ 44]. In this study [ 82], the pathogen-induced mucin production was also suppressed by phloretin. In RAW 264.7 macrophages exposed to COPD associated pathogens ( Moraxella catarrhalis and Streptococcus pneumoniae) and nontypeable Haemophilus influenzae (NTHi)-induced human bronchial epithelial (HBE) cells, the enhanced TNF secretion was suppressed by phloretin (100 µM) [ 44]. The direct effect of phloretin on bacteria should not also rule out as a mechanism contributing to the inhibition of pathogenic bacteria-induced lung inflammation. For example, human alveolar epithelial cell (A549 cells) damage caused by S. aureus in vitro could be ameliorated by phloretin (2–16 µg/mL) perhaps through a mechanism including a direct effect on bacteria such as an effect on the activity of the virulence factors, as shown for sortase B [ 82]. I’ve already told you how Skinceuticals Phloretin CF compares to Skinceuticals CE Ferulic. To me, the latter is the BEST Vitamin C serum on the market (and yes, it makes me cry, it’s so expensive!), so I don’t see the need for more Vitamin C serums. Skinceuticals obviously disagrees with me as they have quite a few options available. Let’s take a look at how Skinceuticals Phloretin CF compares to them:

Once absorbed, this serum can’t be washed or rubbed off. It remains effective for a minimum of 72 hours, making it an excellent addition to sunscreen. Hi, I'm Gio. I'm a no-nonsense, tell-it-like-it-is skin coach and writer on a mission to help you achieve your best skin day ever - every day. I bust skincare myths and debunk marketing jargon to help you figure out what's worth the splurge and what's best left on the shelf - using science, not hype. I also offer skincare consultations to help you create the best skincare routine for your unique needs. Skinceuticals CE Ferulic and Phloretin CF are the two most popular Vitamin C serums from the brand. How do they compare? Helps prevent free radical damage, diminishes the appearance of discolouration and improves skin tone and texture.

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But I love fragrance-free products. Fragrance is one of the most (if not the most) irritating ingredient in skincare products. By taking it out, you greatly lower the risk someone will have an allergic reaction to it. Anti-inflammatory effect of phloretin through inhibition of phosphorylation of MAPKs and IκBα. Most of the studies on the activation of inflammatory mediators from immune cells employed LPS which interacts with its receptor, TLR4. While a direct effect on TLR1/2 has been suggested, most of the data indicate an inhibitory effect on NF-κB mobilization to the nucleus. The LPS response shown by blue arrows includes the degradation of the NF-κB inhibitory protein, IκBα, via promoting its phosphorylation. This frees the p65/p50 to mobilise to the nucleus and activate inflammatory target genes such as COX, iNOS, and cytokines including TNF-α, IL-1β, and IL-6. Phloretin has been shown the suppress the NF-κB activity by inhibiting IκBα degradation (see red lines). The exact mechanism of how the MAPK activity leads to the activation of proinflammatory genes has not yet been fully established but the key steps after induction by inflammatory agents such as LPS is the phosphorylation of p38, ERK, and JNK which have been shown to be targeted by phloretin (see red lines). Note that other pro-inflammatory agents such as TNF-α, IL-1β, and IL-6 can also activate the MAPK and NF-κB pathways by interacting with their cell-surface receptors. Groundbreaking for its day, it has now become the gold standard for Vitamin C serums and inspired a long string of dupes (and lawsuits). Now they’re bringing another innovation, 15% L-Ascorbic Acid (Vitamin C) + Ferulic Acid + Phloretin. Will it be as successful as its predecessor? Only time will tell. Key Ingredients In Skinceuticals Phloretin CF: What Makes It Work?

In the various sections of this review ( Section 2, Section 3, Section 4, Section 5, Section 6, Section 7, Section 8, Section 9, Section 10 and Section 11), the anti-inflammatory potential of phloretin that has been established through studies both in vitro and in vivo are outlined. Indeed, phloretin does also possess various other pharmacological effects including anticancer properties. Readers should bear in mind that carcinogenesis and the process of cancer metastasis including angiogenesis share some aspects of inflammation biology. Hence, the reported anti-inflammatory mechanism of phloretin could also be relevant to its anticancer properties. The focus of this section is however to summarise the anti-inflammatory mechanism of phloretin that accounts for its diverse other effects in vitro and in vivo. 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]. A mineral tinted fluid, this daily sunscreen is suitable for all skin types and instantly helps improve the appearance of uneven skin tone while protecting the skin from further discoloration and damage. Featuring micro-fine zinc oxide (Z-Cote®) and titanium dioxide to provide broad spectrum protection against UVA/UVB rays, this ultra-sheer, non-irritating formula is infused with artemia salina to enhance the skin’s natural defenses against UV- and heat-induced stress, plus translucent color spheres that help even out skin tone and boost skin’s radiance upon application. With a paraben- and fragrance-free, non-comedogenic formula that’s ideal for all skin types (including sensitive), this lightweight, water-resistant fluid provides a touch of coverage and leaves skin with a soft, radiant finish as well as no white cast. For evening use: Retinol 0.3, 0.5 or 1.0 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. 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].Provides advanced environmental protection from skin-damaging free radicals caused by sun and pollution Irritation:High concentrations (%15) of L-Ascorbic Acid – especially at the low pH (below 3) it needs to work its magic – can irritate skin, especially if it’s sensitive. Phloretin CF uses 10%, a concentration that’s sensitive skin-friendly. 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. Inhibits TLR2/1 heterodimerization; reduces TNF-α; and IL-8; exhibits micromolar binding affinity to TLR2.

Increasing the uptake of phloretin in biological systems to improve its efficacy received some attention in recent years. This has also been tried out in inflammation research [ 156] but most of the studies are related to absorption from the skin given the wide application of the compound in skin products. Thus, polymeric nanocapsules loaded with phloretin [ 157], hydrophilic, and other lipophilic formulations [ 158], and absorption from skin lotions [ 159] have been studied. By using mixed polymeric-modified self-nanoemulsions, Wang et al. [ 160] have shown that the water solubility of phloretin can be enhanced 3000-fold, its bioavailability by 7.9-fold, and it is in vivo anti-inflammatory effect by 6.8-fold. The application of fast-dissolving nanofibers [ 161] and nanoparticles [ 162] including chitosan nanoparticles [ 163] for drug-resistant cells in cancer therapy using phloretin formulation has also been explored. Moreover, various other approaches are now adopted to formulate phloretin for a better therapeutic efficacy outcome and more research in this field will solve its limitation in bioavailability.By using the standard ulcerative colitis experimental model in mice induced by dextran sulfate sodium (DSS), Wu et al. [ 87] demonstrated the anti-inflammatory effect of phloretin (60 mg/kg p.o. daily for 7 days) in vivo. The novel feature of this study was faecal microbiota transplantation (FMT) or transferring faecal microbes (10 9 CFU/mL) from phloretin-treated diseased mice by gavage to non-phloretin-treated diseased mice. This FMT, as well as phloretin treatment, ameliorated ulcerative colitis by improving pathological markers (e.g., reversing the shortening of colon length and increased Muc2 mRNA and Claudin-1, zonula occludens-1 (ZO-1) protein expressions) and colon inflammation (suppression of cytokines including TNF-α, IL-6 and IL-1β, NF-κB and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation) and oxidative stress (increase the levels of SOD and GSH and decreasing MDA) markers in colonic tissues. This study which also demonstrated the reversal of the change in the gut microflora population induced by ulcerative colitis supports the hypothesis that some of the phloretin’s effects as an anti-inflammatory agent may be associated with modulation of the gut microbiota structure/population. Further evidence substantiating the link between gut microbiota dysbiosis and ulcerative colitis and the reversal of the disease’s pathology by phloretin came from the study by Liu et al. [ 88]. In DSS-induced ulcerative colitis in mice, treatment with phloretin (100 mg/kg, p.o. for three weeks) was shown to reverse the disease score, inflammatory markers (NF-κB activation), and reverse the change in microbiota population of the gut. In an experiment using a lower dose of phloretin (60 mg/kg, p.o.), the DSS-induced ulcerative colitis score in mice was shown to be correlated with normalising the composition of microbes and their metabolites [ 89]. Phloretin (at concentrations less than 100 µM) is known to inhibit adipogenesis and promote apoptosis in adipocytes in vitro [ 62, 63, 64]. In oleic acid-treated HepG2 cells, it also prevented excessive lipid accumulation and decreased the sterol regulatory element-binding protein 1c (SREBP-1c), inhibiting the expression of fatty acid synthase (FAS), while it increased the sirtuin 1 (SIRT1), and phosphorylation of AMPK to suppress acetyl-CoA carboxylase expression thereby suppressing the synthesis of fatty acids [ 65]. In high-fat-diet (HFD)-fed obese mice, phloretin reduced body weight and fat weight, liver weight and liver lipid accumulation, and improved hepatocyte steatosis. In liver tissue of obese mice, phloretin further suppressed transcription factors of lipogenesis and fatty acid synthase, and increased lipolysis and fatty acid β-oxidation. In addition, phloretin regulated serum leptin, adiponectin, triglyceride, low-density lipoprotein, and free fatty acid levels in obese mice [ 65]. The role of phloretin in lipid metabolism is, however, complex as it also promotes adipocyte differentiation in vitro and improves glucose homeostasis in vivo by increasing the expression of adipose-related genes or adipogenic markers (peroxisome proliferator-activated receptor-γ (PPARγ), CAAT enhancer binding protein-α (C/EBPα), fatty acid synthase, fatty acid-binding protein 4, and adiponectin such as fatty acids translocase and fatty acid synthase [ 64]. In this connection, phloretin is known to enhance adipocyte differentiation and adiponectin expression by mechanisms including PPARγ activation as well as modulation of gene expression with the implication of reducing insulin resistance [ 66]. When RAW 264.7 macrophages were co-cultured with 3T3-L1 cells during adipocytes differentiation, phloretin (and to a very less extent phlorizin) inhibited the adipogenesis-related transcription factors. The phosphorylation of AMPK and the activity of adipose triglyceride lipase and hormone-sensitive lipase were augmented. As an anti-inflammatory compound, phloretin also suppressed the NF-κB and MAPK pathways [ 67]. Its effects on obesity-associated inflammation are further scrutinised below. The best vitamin C serums have the power to promote the skin’s collagen and elastin production, neutralise free radicals from environmental stress, and brighten the complexion – helping to fade and prevent hyperpigmentation. Vitamin C – the ingredient also known as ascorbic acid or l-ascorbic acid – really is an anti-ageing powerhouse, but not all skincare formulas centred on the antioxidant are made equal. 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. One of the main benefits of ascorbic acid is its potent antioxidant activity. Ascorbic acid donates electrons to neutralize free radicals from environmental factors such as UVA/UVB radiation, infrared radiation (IRA), and ozone pollution (O3). This is important because the harmful effects of free radicals occur as direct chemical alterations of the cellular DNA, the cell membrane, and cellular proteins, including collagen. Damaged collagen manifests as signs of premature skin aging, including wrinkles, lines, and sagging skin. By protecting collagen and other skin components, ascorbic acid helps to prevent signs of aging. This is one way that SkinCeuticals Phloretin CF provides advanced environmental protection.

That’s why we recommend considering Formulyst Active Serum, a multi-tasking serum that contains a blend of antioxidant vitamins C and E, ferulic acid, niacinamide, and panthenol to help shield your skin from environmental assaults that age your skin. It’s the ultimate antioxidant formulation to help your skin look brighter, healthier, and more youthful. 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.Vitamin C is a must for anti-aging, but no particular serum is an absolute must – especially at this price point. But if your skin can’t tolerate high doses of Vitamin C (and your wallet can take the hit), this is an effective alternative to consider. Dupes & Alternatives 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.