Mongolians are known as heavy drinkers, and they have a high incidence of essential hypertension, which may be an associated pathology. We examined a possible association of essential hypertension and polymorphism of the aldehyde dehydrogenase 2 (ALDH2) gene in Mongolians from Inner Mongolia. Single nucleotide polymorphism rs671 of ALDH2 was detected by TaqMan PCR in 91 essential hypertensive patients (44 males and 47 females) and 70 healthy Mongolians (37 males and 33 females). Frequencies of the ALDH2*1/1 genotype and the ALDH2*1 allele in patients (91.2 and 95.6%, respectively) were significantly higher than in controls (78.6 and 89.3%; P < 0.05), while frequencies of ALDH2*1/2 genotype and ALDH2*2 allele in patients (8.79 and 4.4%) were much lower than in controls (21.4 and 10.7%; P < 0.05). Frequencies of ALDH2*1/1 genotype and ALDH2*1 allele in female patients (95.8 and 94.9%) were higher than in female controls (70.0 and 84.9%; P < 0.05); frequencies of the ALDH2*1/2 genotype and the ALDH2*2 allele in female patients (4.25 and 2.13%) were lower than in female controls (30.3 and 15.2%, P < 0.05). There was no significant difference in male subjects. ALDH2*2/2 was not found in any of the subjects. We conclude that ALDH2 polymorphism is associated with essential hypertension in Mongolians, especially in female Mongolians. ALDH2*2 was found to be a negative risk factor for essential hypertension in Mongolians from Inner Mongolia.

Background: Acne is a chronic facial disease caused by Propionibacterium acnes, which proliferates within sebum-blocked skin follicles and increases inflammatory cytokine production. Several therapeutic drugs and products have been proposed to treat acne, yet no single treatment that ensures long-term treatment efficacy for all patients is available. Here, we explored the use of facial autologous fat transplant of adipose-derived stem cells (ADSCs) to dramatically reduce acne lesions. Methods: THP-1 cells were treated with active P. acnes for 24 h at different multiplicities of infection, and alterations in inflammatory factors were detected. To study the effect of THP-1 on inflammasome-related proteins, we first co-cultured ADSCs with THP-1 cells treated with P. acnes and evaluated the levels of these proteins in the supernatant. Further, an acne mouse model injected with ADSCs was used to assess inflammatory changes. Results: Propionibacterium acnes-mediated stimulation of THP-1 cells had a direct correlation with the expression of active caspase-1 and interleukin (IL)-1β in an infection-dependent manner. ADSCs significantly reduced the production of IL-1β induced by P. acnes stimulation through the reactive oxygen species (ROS)/Nod-like receptor family pyrin domain-containing 3 (NLRP3)/caspase-1 pathway. The results showed that ADSCs inhibit the skin inflammation induced by P. acnes by blocking the NLRP3 inflammasome via reducing the secretion of IL-1β in vivo. Conclusions: Our findings suggest that ADSCs can alter IL-1β secretion by restricting the production of mitochondria ROS, thereby inhibiting the NLRP3/caspase-1 pathway in P. acnes-induced inflammatory responses. This study indicates that anti‐acne therapy can potentially be developed by targeting the NLRP3 inflammasome.

Background: Acute radiation-induced dermatitis refers to skin lesions that usually appear within 90 days of the start of radiotherapy. Although various treatments are available, none have proven fully effective. Exosomes produced by adipose-derived stem cells play crucial roles in enhancing cell regeneration, promoting angiogenesis, regulating inflammation and remodeling the extracellular matrix. Hyaluronic acid, a major extracellular matrix component, is synthesized by hyaluronic acid synthase, with hyaluronic acid synthase 1 being particularly critical for skin repair. This study aimed to investigate whether exosomes derived from adipose-derived stem cells can protect against radiation-induced acute skin damage and to elucidate the underlying mechanisms involving hyaluronic acid synthase 1. Methods: Thirty-six male adult SD rats were randomly divided into a negative control group, an irradiation group (90 Gy), and a radiation + exosomes group (90 Gy + 100 ug exosomes). Three groups of fibroblasts were assigned: one for control, one for radiation (6 Gy), and one for radiation plus exosomes (6 Gy + 4 ug exosomes). The effect of ADSC-exos transplantation was evaluated using skin damage score, histopathological analysis, electron microscopy, immunohistochemical staining, immunofluorescence staining, and immunoblotting analysis. Furthermore, small interfering RNA-mediated knockdown of hyaluronic acid synthase 1 was performed to explore its regulatory role in the TGF-β/Smad2/3 signaling pathway. Results: After irradiation, the ADSC-exos intervention significantly increased the levels of stromal cell-derived factor-1, matrix metalloproteinases, transforming growth factor, basic fibroblast growth factor, platelet-derived growth factor, vascular endothelial growth factor, interleukin 10, interleukin 12, and reduced the expression of the pro-inflammatory factor interleukin 6. Notably, exosomes treatment markedly upregulated hyaluronic acid synthase 1 expression, and small interfering RNA-mediated knockdown of hyaluronic acid synthase 1 resulted in reduced phosphorylation of TGF-β/Smad2/3 signaling components, indicating that hyaluronic acid synthase 1 is a critical mediator of this pathway. Conclusion: Exosomes derived from adipose-derived stem cells alleviate acute radiation-induced dermatitis by enhancing hyaluronic acid synthase 1 expression and activating the TGF-β/Smad2/3 pathway, thereby promoting skin regeneration and repair. These findings suggest that exosomes derived from adipose-derived stem cells may serve as a promising cell-free therapeutic strategy for the prevention and treatment of acute radiation-induced dermatitis. Graphical

Background: Keloid is a fibroproliferative disease with unsatisfactory therapeutic effects and a high recurrence rate. exosomes produced by adipose-derived mesenchymal stem cells (ADSC-Exos) have attracted significant interest due to their ability to treat fibrosis. However, the molecular mechanisms of ADSC-Exos in keloids remain inconclusive. Objective: Our study revealed the relationship between ferroptosis and fibrosis in keloids. Subsequently, this study aimed to explore further the anti-fibrotic effect of ADSC-Exos on keloids through ferroptosis and the potential underlying mechanisms. Methods: To investigate the impact of ferroptosis on keloid fibrosis, Erastin and ferrostatin-1 (fer-1) were utilized to treat keloid fibroblast. Keloid keloids treated with Erastin and fer-1 were cocultured with ADSC-Exos to validate the impact of ferroptosis on the effect of ADSC-Exos on keloid anti-ferrotic protein, peroxidase 4 (GPX4) and anti-fibrotic effects in vivo and in vitro by Western blot, as well as variations in iron metabolite expression, malondialdehyde (MDA), liposomal peroxidation (LPO) and glutathione (GSH) were analyzed. The effect of solute carrier family 7-member 11 (SLC7A11) silencing on ADSC-Exo-treated keloid fibroblast was investigated. Results: Iron metabolite dysregulation was validated in keloids. Fibrosis progression is enhanced by Erastin-induced ferroptosis. The anti-fibrotic effects of ADSC-Exos and fer-1 are related to their ability to prevent iron metabolism. ADSC-Exos effectively suppressed keloid fibrosis progression and increased GSH and GPX4 gene expression. Additionally, the use of Erastin limits the effect of ADSC-Exos in keloids. Furthermore, the effect of ADSC-Exos on keloids was associated with SLC7A11-GPX4 signaling pathway. Conclusion: We demonstrated a new potential mechanism by which anti-ferroptosis inhibits the progression of keloid fibrosis and identified an ADSC-Exo-based keloid therapeutic strategy. Resisting the occurrence of ferroptosis and the existence of the SLC7A11-GPX4 signaling pathway might serve as a target for ADSC-Exos.