Effect Of Azelaic Acid Research Articles

Effect of Azelaic Acid on Psoriasis Progression Investigated Based on Phosphatidylinositol 3-Kinase (PI3K)/Protein Kinase B (AKT) Signaling Pathway.

To probe into the effect of azelaic acid on psoriasis based on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Psoriasis gene expression data were downloaded from the GEO database for differential expression analysis to identify differentially expressed genes (DEGs). KEGG and GSEA analyses were performed to identify important signaling pathways that may be involved in psoriasis progression for subsequent validation. Thirty-six C57BL/6 mice aged 8 weeks old were randomly assigned into the blank control group (n = 9), negative control group (n = 9), psoriasis model group (n = 9), and azelaic acid treat group (n = 9). Mice models of psoriasis were prepared with imiquimod (IMQ) in the latter two groups, and azelaic acid ointment was applied in azelaic acid treat group. Then, hematoxylin-eosin (HE) staining was carried out to detect the effect of azelaic acid on the pathological damage of mice models of psoriasis in each group. HaCaT cells cultured in vitro were divided into blank control group, negative control group (addition of azelaic acid), IL-17 group (20 ng/mL) and IL-17+azelaic acid group, with 3 replicates for each group. Immunofluorescence assay and Western blotting were used to detect the protein expression of PI3K/AKT signaling pathway related molecules. KEGG analysis showed that DEGs were significantly enriched in PI3K-AKT signaling pathway. GSEA analysis showed that PI3K and MTOR signaling pathways were up-regulated in psoriasis, while AUTOPHAGY signaling pathway was down-regulated. HE staining showed that azelaic acid could significantly inhibit the local skin injury in mice caused by IMQ-induced psoriasis. Moreover, azelaic acid can inhibit the expression of PI3K/AKT signaling pathway related proteins phosphorylated (p)-PI3K, p-AKT, p-mammalian target of rapamycin (mTOR), vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2), angiogenin-1 and hypoxia-inducible factor-1α (HIF-1α). These results imply that azelaic acid may inhibit the activation of PI3K/AKT signaling pathway and angiogenesis, thereby improving the symptoms of psoriasis. Azelaic acid may inhibit the activation of PI3K/AKT signaling pathway and angiogenesis, thereby improving the symptoms of psoriasis.

The Effect of Azelaic Acid and Vitamin C on the Stability of Hydroquinone in Extemporaneous Topical Preparations: an Evidence-Based In Vitro Research

Research has shown that co-administration of preparations containing HQ and azelaic acid (AZ) or vitamin C (vit C) may be more effective than HQ alone. The aim of this study was to evaluate the stability of HQ in the presence of AZ and vit C as active ingredients in the extemporaneous preparations prepared with different techniques. Topical preparations containing HQ, vit C, and AZ were prepared using with aqueous and none-aqueous extemporaneous techniques. Some auxiliary antioxidants were used to stabilize vit C. Thermal stress condition was applied for stability evaluation. Digital images and HPLC analysis were performed to control the color changes and drug loss, respectively. Severe color changes happened in some formulations and dark brown color appeared. Color change was directly attributed to vit C loss but not related to HQ loss. HQ ointment with no antioxidant, showed no loss after stress incubation. AZ was partially able to increase the HQ and vit C stability in a combination formulation, but this stabilizing effect in binary formulations of HQ and AZ was not seen. SMB enhanced vit C stability. Aqueous preparation methods decreased the stability of formulations significantly. It can be recommended that HQ, vit C, and AZ be formulated in separate dosage forms. Avoiding water incorporating or aqueous methods will enhance the stability of these formulations, as well. Intrinsic low stability of vit C in topical formulations may be enhanced using non-water incorporating or non-aqueous methods and utilizing SMB in suitable concentrations.

Effect of azelaic acid on microstructure evolution and electrical properties of anodic aluminum foil for electrolytic capacitor

The effect of azelaic acid on microstructure evolution and electrical properties of anodic aluminum foil for electrolytic capacitor is studied quantitatively. The azelaic acid is selected as formation solution in the multi-step anodization process, and boric acid is applied for comparison. The field-emission scanning electron microscopy and X-ray diffractometer technologies are used for observation of microstructure and detection of crystallinity, respectively. The electrical properties are tested by LCR meter and T–V tester. The microstructure observation shows that the ‘corn-flake’ structures are taken place by ‘cotton-ball’ ones gradually along with the preparation process, and such phenomenon is more obvious when azelaic acid is used. The pores area of anodic aluminum foil formed in azelaic acid is larger because of the stronger acidity. The formation with azelaic acid induces smaller thickness of oxide film, promotes the formation of crystalline oxide, therefore, a barrier film with higher crystallinity and larger grain size is obtained. The barrier film formed in azelaic acid shows larger specific capacitance, lower withstand voltage and larger leakage current, which needs the multi-step anodization for performance improvement.

AZELAIC ACID ATTENUATESROTENONE-INDUCED BEHAVIOURAL ALTERATIONS IN PARKINSON’S DISEASE RAT MODEL

In the current study, we investigated the anti-Parkinson’s effect of azelaic acid (AA; 20 mg/kg, 40mg/kg, 80 mg/kg p.o.) against rotenone (2 mg/kg s.c.) induced Parkinson’s disease (PD) rat model. Rotenone was administered continuously for 35 days and caused behavioural alterations such as catalepsy, rigidity in muscles, posture instability and decrease in body weight, locomotor activity, and rearing behaviour.AAshowed significant (p<0.05) reversal in behavioural alterations induced by rotenone at 80 mg/kg dose on 28th and 35th day of treatment. Administration of azelaic acid along with levodopa-carbidopa (100mg/kg+25mg/kg p.o.) also showed significant reversal of behavioural alterations induced by rotenone and this effect was comparable to the effect of levodopa-carbidopa treatment group. The study proved the ameliorative effect of azelaic acidin rotenone induced PD rat model indicating its possible therapeutic potential for this devastating disease.

The role and place of azelaic acid in the routes of patients with acne vulgaris

The review presents data from foreign and domestic clinical studies on the efficacy and safety of azelaic acid (Skinoren) in the treatment of acne vulgaris. New aspects of pathogenesis are presented, an analysis of the database of systematic reviews of Russian, European, American researchers is presented, including an analysis of the database of systematic reviews of the Cochrane Systematic Review Intervention Version of the Cochrane Skin Group (2020) comparative studies on the effectiveness of azelaic acid, Skinoren and other topical topical medications for the treatment of acne vulgaris. Possibilities of monotherapy with the preparation of azaelaic acid Skinoren and variants of combined treatment, in particular, a combination of azelaic acid with topical retinoids, benzoyl peroxide, systemic and topical antibiotics for the treatment of acne of varying severity, are shown. Reliable efficacy, safety, the possibility of long-term therapy, high compliance allow us to conclude that Skinoren is highly effective in treating acne, and a number of priority complex advantages, such as the presence of anti-inflammatory, antibacterial, anti-keratinizing, antiandrogenic and anti-tyrosinase action, allow Skinoren to be considered as optimal. topical agent for long-term and safe treatment of acne and prevention of the development of post-acne symptom complex.

The role and place of azelaic acid in the routes of patients with acne vulgaris

The review presents data from foreign and domestic clinical studies on the efficacy and safety of azelaic acid (Skinoren) in the treatment of acne vulgaris. New aspects of pathogenesis are presented, an analysis of the database of systematic reviews of Russian, European, American researchers is presented, including an analysis of the database of systematic reviews of the Cochrane Systematic Review Intervention Version of the Cochrane Skin Group (2020) comparative studies on the effectiveness of azelaic acid, Skinoren and other topical topical medications for the treatment of acne vulgaris. Possibilities of monotherapy with the preparation of azaelaic acid Skinoren and variants of combined treatment, in particular, a combination of azelaic acid with topical retinoids, benzoyl peroxide, systemic and topical antibiotics for the treatment of acne of varying severity, are shown. Reliable efficacy, safety, the possibility of long-term therapy, high compliance allow us to conclude that Skinoren is highly effective in treating acne, and a number of priority complex advantages, such as the presence of anti-inflammatory, antibacterial, anti-keratinizing, antiandrogenic and anti-tyrosinase action, allow Skinoren to be considered as optimal. topical agent for long-term and safe treatment of acne and prevention of the development of post-acne symptom complex.

Azelaic acid stimulates catalase activation and promotes hair growth through upregulation of Gli1 and Gli2 mRNA and Shh protein.

Although azelaic acid is effective for treatment of acne and rosacea, the biological activity of azelaic acid and the effect of its combination therapy with minoxidil were not elucidated with regard to hair growth. In this study, mouse vibrissae follicles were dissected on day 10 after depilation. Then, the bulb and bulge cells of the hair follicle were treated with minoxidil and azelaic acid for 10 days to evaluate Sonic hedgehog (Shh) protein expression. Moreover, bulge and bulb cells of the hair follicles were cultivated and the expression of Gli1, Gli2, and Axin2 mRNA levels was evaluated using real-time polymerase chain reaction(PCR) analysis. We further investigated the protective effects ofazelaic acid againstultraviolet B (UVB)irradiation in cultured bulb and bulge cells by determining catalase activity. An irradiation dose of 20 mJ/cm2UVB for 4 sec was chosen. The results showed that catalase activity significantly (p<0.05) increased in the bulge cells after exposure to 2.5 mM and 25 mM azelaic acid. Meanwhile, treatment of the bulb cells with azelaic acid (2.5 and 25 mM) did not cause significant changes in catalase activity. We also found that azelaic acid (25 mM) alone upregulated Gli1 and Gli2 expression in the bulge cells and 100 µ minoxidil caused Gli1 and Axin2 overexpression in the bulb region of the hair follicle. Moreover, minoxidil (100 µM) alone and in combination with azelaic acid (25 mM) led to Shh protein overexpression in the hair follicles in vitro and in organ culture. Our results indicated a potential role for azelaic acid in the protection of bulge cells from UVB damage and its combination with minoxidil may activate hair growth through overexpression of Shh protein.

Azelaic acid accumulates in phloem exudates of TMV-infected tobacco leaves, but its application does not induce local or systemic resistance against selected viral and bacterial pathogens

Local and systemic effects of azelaic acid (AzA) pretreatments on local necrotic lesion formation induced by Tobacco mosaic virus (TMV) were studied in Nicotiana tabacum cv. Xanthi nc plants as measured by a semi-automated, computer-assisted method. Local application of AzA (0.2–1.0 mM) showed no or limited influence (either increase or decrease) on lesion size of TMV-inoculated leaves. In addition, AzA pretreatment did not modify the multiplication of TMV detected by semiquantitative RT-PCR. No significant systemic effect of AzA on lesion size of TMV was detectable in distant leaves. Moreover, AzA treatment had no considerable local and systemic effect on symptom expression and multiplication of incompatible (P. syringae pv. tomato DC3000) and compatible (P. syringae pv. tabaci) bacteria. The response of the viral and bacterial pathogens to AzA was not different if tobacco plants were exposed to light or darkness after AzA treatment. However, the amount of AzA, measured by HPLC–MS, was doubled in phloem exudates of TMV infected leaves as compared to the control leaves, but concentrated exudates containing AzA did not induce local resistance response. In addition, the amounts of two other short-chain dicarboxylic acids (suberic acid and sebacic acid) increased in phloem exudates of virus-infected leaves. All these results suggest that, at least in tobacco, AzA does not induce considerable local or systemic effects on viral and bacterial infections. Therefore, its formerly reported role in signal transduction and/or induction of systemic acquired resistance (SAR) in Arabidopsis cannot be confirmed in tobacco.

Effect of azelaic acid on melanoma cells in culture

Using a clonogenic assay in vitro, it has been shown that exposure to azelaic acid (1-100 mM) for 24 hours has a dose-dependent effect on the survival of the colony-forming ability of murine (B16) and human (HMB2, and SK23) melanoma cells as compared with a non-melanotic non-tumoral Chinese hamster cell line (CHO). Both human cell lines were more sensitive to the diacid than the murine cells, and the HMB2 cells were more sensitive than the SK23 cells. These differences may be partly correlated with differences in pigmentation and doubling times between the three melanoma cell lines. The two human lines were more pigmented than the B16, and the SK23 more than the HMB2; the human lines had a longer doubling time than the others.

The depigmenting effect of azelaic acid

The depigmenting effect of azelaic acid

Effects of Azelaic Acid on Proliferation and Ultrastructure of Mouse Keratinocytes in Vitro

The effects of azelaic acid (C9-dicarboxylic acid, AZA) on the proliferation and ultrastructure of neonatal NMRI mouse keratinocyte cultures were studied to clarify the mechanisms of AZA action on normal and diseased epidermis. The dose- and time-dependency of the drug effects on DNA synthesis was examined by 3H-thymidine incorporation into DNA and by autoradiography. Electron microscopy was used to detect the target cell organelles of the drug. Azelaic acid decreased DNA synthesis in a dose- and time-dependent manner with a 50% inhibitory concentration of 20 mM. The inhibition of DNA synthesis was already observed after 1 h of treatment, reached its maximum after 4 h, and was stable for 24 h. A complete reversibility of the inhibitory effects was observed within 2 h after discontinuation of the treatment, and, interestingly, a rebound effect occurred with a temporary increase of DNA synthesis. Furthermore, treatment with AZA reduced the RNA and protein synthesis of the cells. Electron microscopic evaluation of treated cultures showed early marked damage of the mitochondria, followed by dilation of the rough endoplasmic reticulum (RER). These alterations were completely reversible after discontinuation of the treatment. Our findings show that AZA exerts a dose- and time-dependent, reversible antiproliferative effect on keratinocytes, acting primarily on mitochondria and RER. The antiproliferative action of AZA could explain its beneficial effect in some skin disorders characterized by alteration of keratinocytic differentiation.

The effect of azelaic acid on cutaneous bacteria

(1989). The effect of azelaic acid on cutaneous bacteria. Journal of Dermatological Treatment: Vol. 1, No. sup1, pp. 17-19.

Ultrastructural observations on the effect of azelaic acid on normal human melanocytes and a human melanoma cell line in tissue culture.

Azelaic acid has been shown clinically to have a cytotoxic effect on the abnormally active and malignant human melanocyte, but it has no apparent effect upon normal melanocytes. This difference in reactivity between normal and abnormal cells in vivo is further examined here in vitro. The disodium salt of azelaic acid (C(9)2Na) was added to pure and mixed cultures of normal human melanocytes and to cultured human melanoma cells, at 10(-3) M, 10(-2) M, 5 X 10(-2) M, and 10(-1) M for 1 and 6 h. Control cultures and cultures exposed to the same concentrations of the disodium salt of adipic acid (C(6)2Na) were also examined. No damage to cells of any line was observed with diacids at 10(-3) M or 10(-2) M up to 6 h. At 5 X 10(-2) M some mitochondria of melanoma cells appeared swollen. With C(6)2Na at 10(-1) M for I and 6 h, minimal swelling of mitochondria was observed in some cells of all lines. Pure normal melanocytes and melanocytes of mixed cultures exhibited greater swelling of mitochondria with 10(-1) M C(9)2Na at 1 and 6 h, but the mitochondria of the malignant melanocytes were massively swollen with destruction of cristae. Plasma and nuclear membranes and membranes of rough endoplasmic reticulum were intact, but Golgi membranes exhibited vesiculation. These results provide further evidence that azelaic acid damages the human malignant melanocyte and that one of its targets is the mitochondrion. Damage to normal melanocytes, found here, may be due to the fact that, in culture, they are more active than in intact epidermis.