Salvianolic Acid B Reduces Oxidative Stress to Promote Hair-Growth in Mice, Human Hair Follicles and Dermal Papilla Cells.

Background: Existing research links oxidative stress and inflammation to hair loss. Salvianolic acid B (SAB) is known for its anti-oxidative, anti-inflammatory, and other beneficial pharmacological properties. Objective: To assess the efficacy of SAB in modulating hair growth. Methods: In vivo experiments were conducted using C57BL/6 mice to evaluate the effects of SAB on hair and skin parameters. The study involved ex vivo analysis of human hair follicles (HFs) for hair shaft length and hair growth cycle assessment. In vitro, human dermal papilla cells (hDPCs) were cultured with SAB, and their proliferation, protection against H2O2-induced oxidative damage, and gene/protein expression alterations were examined using various analytical techniques, including Real-Time Cell Analysis (RTCA), DCFH-DA Assay, RNA-seq, and KEGG pathway analysis. Results: SAB treatment in mice significantly improved hair growth and vascularization by day 21. In human HFs, SAB extended hair shaft length and delayed the transition to the catagen phase. SAB-treated hDPCs showed a notable decrease in the expression of oxidation-antioxidation-related genes and proteins, including reduced phosphorylation levels of ERK and p38. Conclusion: The study indicates that SAB promotes hDPC proliferation and offers protection against oxidative stress, highlighting its potential as a therapeutic agent for enhancing hair growth and treating hair loss.

Clinicopathological characteristics of fibrosing alopecia in a pattern distribution: a single-center, retrospective study.

BACKGROUND: Fibrosing alopecia in a pattern distribution (FAPD) is a distinct entity of primary cicatricial alopecia (PCA), mimicking diffuse hair loss of androgenetic alopecia (AGA) with trichoscopic and histopathologic features of both AGA and lichen planopilaris (LPP). METHODS: Clinical, demographic, and histopathological data of 20 FAPD patients were retrospectively collected. RESULTS: All patients presented with female pattern hair loss with a median Sinclair grade of 3. Trichoscopic findings revealed hair diameter variability (20/20), perifollicular erythema (mild 7/20, moderate 11/20, severe 2/20), peripilar casts (none 2/20, mild 12/20, moderate 5/20, severe 1/20), and loss of follicular ostia (+12/20, ±7/20, -1/20). Histopathologic examination revealed perifollicular lymphocytic infiltration at the infundibulum or isthmus level and an increase of vellus-like hairs. All cases showed interface dermatitis with concentric perifollicular lamellar fibrosis and follicular scars. Infundibular or isthmic infiltration of mast cells was found. CONCLUSIONS: The uniqueness of our study lies in perifollicular mast cells and discovering that the young population is at higher risk than previously thought. Clinicopathological features of FAPD were identified, filling the void of much-needed details for FAPD diagnosis tailored to the Chinese population.

ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L.

This study aimed to investigate whether annexin A7 (ANXA7) could promote the cell cycle, proliferation and cell adhesion-mediated drug resistance (CAM-DR) of multiple myeloma (MM) cells by up-regulating cell division cycle 5-like (CDC5L). As a result, ANXA7 expression was increased in the serum of MM patients and the expression of ANXA7 and CDC5L was also increased in MM cell lines. ANXA7 overexpression promoted the proliferation and cycle of U266 and RPMI8226 cells. The expression of proliferation cell nuclear antigen (PCNA), KI67, cyclin dependent kinase 1 (CDK1) and cyclinB1 in transfected cells was consistent with the changes of proliferation and cell cycle. In co-culture system of BMSC cells and MM cells, expression of CD44, ICAM1 and VCAM1 in MM cells was increased, which was further increased by ANXA7 overexpression. Bortezomib could increase the apoptosis of U266 and RPMI8226 cells. In co-culture system of BMSC cells and MM cells, the promotion effects of bortezomib on apoptosis of MM cells was decreased, which was further suppressed by ANXA7 overexpression. The above effects exerted by ANXA7 overexpression could be reversed by ANXA7 interference. Moreover, ANXA7 was proved to be combined with CDC5L. CDC5L interference could inhibit the promotion effects of ANXA7 overexpression on proliferation and cell cycle and inhibition effects of ANXA7 overexpression on apoptosis of MM cells treated with bortezomib in co-culture system. In conclusion, ANXA7 could promote the cell cycle, proliferation and CAM-DR of MM cells by up-regulating CDC5L.

Type 2 diabetes mellitus does not increase the risk of multiple myeloma: a systematic review and meta-analysis.

BACKGROUND: Epidemiological studies have shown that patients with type 2 diabetes mellitus (T2DM) are at a higher risk of secondary tumors. However, no consensus has been made about whether T2DM can increase the risk of multiple myeloma (MM). METHODS: We searched the databases of PubMed, Cochrane Library and EMBASE and cross-checked the bibliography. Data quality was assessed using the Newcastle-Ottawa scale (NOS). Heterogeneity was calculated as the odds ratio (OR) using a random-effects model. Data were analyzed using Stata version 12.0 software. RESULTS: A total of 13 articles were selected into this meta-analysis. Initially, we found that diabetic patients had a higher risk of myeloma than non-diabetic patients (OR =1.60, 95% CI: 1.13-2.26, I2=98%, P=0.000). But the data in these articles were highly heterogeneous (I2>75%). Therefore, eight of the included articles showed a moderate heterogeneity (I2=71.6%). We used Galbraith heterogeneity map to analyze the causes of heterogeneity. Two articles with high heterogeneity were excluded. Then, we found the heterogeneity of the left six articles was reduced from moderate to mild (I2=45.9%, P=0.100). The final results of this meta-analysis showed that T2DM was not a risk factor for increased incidence of MM (OR =1.05, 95% CI: 0.83-1.33, I2=45.9%, P=0.100). Also, the subgroup analysis (case-control studies vs. cohort studies) showed no statistical difference (OR =1.19, 95% CI: 0.76-1.85, I2=1%, P=0.364; OR =1.00, 95% CI: 0.75-1.33, I2=71.2%, P=0.031; respectively). CONCLUSIONS: T2DM is not a risk factor for the increased incidence of MM, a finding that should be validated with more strictly designed randomized controlled trials (RCTs).