Flavonoid compounds and their synergistic effects: Promising approaches for the prevention and treatment of psoriasis with emphasis on keratinocytes - A systematic and mechanistic review.

Psoriasis, a chronic autoimmune skin disorder, causes rapid and excessive skin cell growth due to immune system dysfunction. Numerous studies have shown that flavonoids have anti-psoriatic effects by modulating various molecular mechanisms involved in inflammation, cytokine production, keratinocyte proliferation, and more. This study reviewed experimental data reported in scientific literature and used network analysis to identify the potential biological roles of flavonoids' targets in treating psoriasis. 947 records from Web of Sciences, ScienceDirect database, Scopus, PubMed, and Cochrane library were reviewed without limitations until June 26, 2023. 66 articles were included in the systematic review. The ten genes with the highest scores, including interleukin (IL)-10, IL-12A, IL-1ß, IL-6, Tumor necrosis factor-α (TNF-α), Janus kinase 2 (JAK 2), Jun N-terminal kinase (JUN), Proto-oncogene tyrosine-protein kinase Src (SRC), Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), and Signal transducer and activator of transcription 3 (STAT3), were identified as the hub genes. KEGG pathway analysis identified connections related to inflammation and autoimmune responses, which are key characteristics of psoriasis. IL-6, STAT3, and JUN's presence in both hub and enrichment genes suggests their important role in flavonoid's effect on psoriasis. This comprehensive study highlights how flavonoids can target biological processes in psoriasis, especially when combined for enhanced effectiveness.

Assessment of GSTO1 (A140D) and GSTO2 (N142D) Gene Polymorphisms in Iranian Women with Polycystic Ovarian Syndrome.

BACKGROUND: Glutathione S-transferases (GSTs) protect cells from oxidative stress (OS). In humans, the GST omega class contains two expressed genes, GSTO1 and GSTO2. Because OS is involved in the pathogenesis of polycystic ovary syndrome (PCOS), the aim of this study was to investigate the relationship between GSTO1 A140D (rs4925) and GSTO2 N142D (rs156697) polymorphisms in PCOS patients. METHODS: 175 PCOS patients and 161 healthy controls were selected among women in Kermanshah province, Iran. GSTO1 and GSTO2 were genotyped using allele-specific PCR (AS-PCR) and PCR-RFLP, respectively. RESULTS: For GSTO1, the DD genotype and the D allele led to 2.17- (P= 0.02) and 1.5-fold (P= 0.01) increases, respectively, in the odds ratios for PCOS. No significant difference was found between control and patient groups for the GSTO2 N142D genotype or allele frequency. GSTO1 and GSTO2 genotype interaction analysis showed that individuals with the GSTO1 AD or DD genotypes and the GSTO2 NN or DN genotypes had a 1.53-fold (P= 0.007) increase in PCOS risk over GSTO1 AA and GSTO2 DD individuals. CONCLUSION: The GSTO1 A140D polymorphism is a risk factor for PCOS.