Capsaicin combined with stem cells improved mitochondrial dysfunction in PIG3V cells, an immortalized human vitiligo melanocyte cell line, by inhibiting the HSP70/TLR4/mTOR/FAK signaling axis.

BACKGROUND: Vitiligo is a common autoimmune skin disease. Capsaicin has been found to exert a positive effect on vitiligo treatment, and mesenchymal stem cells (MSCs) are also confirmed to be an ideal cell type. This study aimed to explore the influence of capsaicin combined with stem cells on the treatment of vitiligo and to confirm the molecular mechanism of capsaicin combined with stem cells in treating vitiligo. METHODS AND RESULTS: PIG3V cell proliferation and apoptosis were detected using CCK-8 and TUNEL assays, MitoSOX Red fluorescence staining was used to measure the mitochondrial ROS level, and JC-1 staining was used to detect the mitochondrial membrane potential. The expression of related genes and proteins was detected using RT‒qPCR and Western blotting. Coimmunoprecipitation was used to analyze the protein interactions between HSP70 and TLR4 or between TLR4 and mTOR. The results showed higher expression of HSP70 in PIG3V cells than in PIG1 cells. The overexpression of HSP70 reduced the proliferation of PIG3V cells, promoted apoptosis, and aggravated mitochondrial dysfunction and autophagy abnormalities. The expression of HSP70 could be inhibited by capsaicin combined with MSCs, which increased the levels of Tyr, Tyrp1 and DCT, promoted the proliferation of PIG3V cells, inhibited apoptosis, activated autophagy, and improved mitochondrial dysfunction. In addition, capsaicin combined with MSCs regulated the expression of TLR4 through HSP70 and subsequently affected the mTOR/FAK signaling pathway CONCLUSIONS: Capsaicin combined with MSCs inhibits TLR4 through HSP70, and the mTOR/FAK signaling pathway is inhibited to alleviate mitochondrial dysfunction and autophagy abnormalities in PIG3V cells.

Enabling Visible-Light-Charged Near-Infrared Persistent Luminescence in Organics by Intermolecular Charge Transfer.

Visible light is a universal and user-friendly excitation source; however, its use to generate persistent luminescence (PersL) in materials remains a huge challenge. Herein, the concept of intermolecular charge transfer (xCT) is applied in typical host-guest molecular systems, which allows for a much lower energy requirement for charge separation, thus enabling efficient charging of near-infrared (NIR) PersL in organics by visible light (425-700 nm). Importantly, NIR PersL in organics occurs via the trapping of electrons from charge-transfer aggregates (CTAs) into constructed trap states with trap depths of 0.63-1.17 eV, followed by the detrapping of these electrons by thermal stimulation, resulting in a unique light-storage effect and long-lasting emission up to 4.6 h at room temperature. The xCT absorption range is modulated by changing the electron-donating ability of a series of acenaphtho[1,2-b]pyrazine-8,9-dicarbonitrile-based CTAs, and the organic PersL is tuned from 681 to 722 nm. This study on xCT interaction-induced NIR PersL in organic materials provides a major step forward in understanding the underlying luminescence mechanism of organic semiconductors and these findings are expected to promote their applications in optoelectronics, energy storage, and medical diagnosis.

Constructing cuprous oxide-modified zinc tetraphenylporphyrin ultrathin nanosheets heterojunction for enhanced photocatalytic carbon dioxide reduction to methane.

The application of supermolecular naonostructures in the photocatalytic carbon dioxide reduction reaction (CO2RR) has attracted increasing attentions. However, it still faces significant challenges, such as low selectivity for multi-electron products and poor stability. Here, the cuprous oxide (Cu2O)-modified zinc tetraphenylporphyrin ultrathin nanosheets (ZnTPP NSs) are successfully constructed through the aqueous chemical reaction. Comprehensive characterizations confirm the formation of type-II heterojunction between Cu2O and ZnTPP in Cu2O@ZnTPP, and the electron transfer from Cu2O to ZnTPP through the Zn-O-Cu bond under the static contact. Under the visible-light irradiation (λ > 420 nm), the optimized Cu2O@ZnTPP sample as catalyst for photocatalytic CO2RR exhibits the methane (CH4) evolution rate of 120.9 µmol/g/h, which is âˆ¼ 4 and âˆ¼ 10 times those of individual ZnTPP NSs (28.0 µmol/g/h) and Cu2O (12.8 µmol/g/h), respectively. Meanwhile, the CH4 selectivity of âˆ¼ 98.7 % and excellent stability can be achieved. Further experiments reveal that Cu2O@ZnTPP has higher photocatalytic conversion efficiency than Cu2O and ZnTPP NSs, and the photoinduced electron transfer from ZnTPP to Cu2O can be identified via the path of ZnTPP→ (ZnTPP•ZnTPP)*→ ZnTPP-→ Zn-O-Cu â†’ Cu2O. Consequently, Cu2O@ZnTPP exhibits a shorter electron-hole separation lifetime (3.3 vs. 9.3 ps) and a longer recombination lifetime (23.1 vs. 13.4 ps) than individual ZnTPP NSs. This work provides a strategy to construct the organic nanostructures for photocatalytic CO2RR to multi-electron products.

Toxic effect and mRNA mechanism of moon dust simulant induced pulmonary inflammation in rats.

Moon dust presents a significant hazard to manned moon exploration missions, yet our understanding of its toxicity remains limited. The objective of this study is to investigate the pattern and mechanism of lung inflammation induced by subacute exposure to moon dust simulants (MDS) in rats. SD rats were exposed to MDS and silica dioxide through oral and nasal inhalation for 6 hours per day continuously for 15 days. Pathological analysis indicated that the toxicity of MDS was lower than that of silica dioxide. MDS led to a notable recruitment and infiltration of macrophages in the rat lungs. Material characterization and biochemical analysis revealed that SiO2, Fe2O3, and TiO2 could be crucial sources of MDS toxicity. The study revealed that MDS-induced oxidative stress response can lead to pulmonary inflammation, which potentially may progress to lung fibrosis. Transcriptome sequencing revealed that MDS suppresses the PI3K-AKT signaling pathway, triggers the Tnfr2 non-classical NF-kB pathway and IL-17 signaling pathway, ultimately causing lung inflammation and activating predominantly antioxidant immune responses. Moreover, the study identified the involvement of upregulated genes IL1b, csf2, and Sod2 in regulating immune responses in rat lungs, making them potential key targets for preventing pulmonary toxicity related to moon dust exposure. These findings are expected to aid in safeguarding astronauts against the hazardous effects of moon dust and offer fresh insights into the implications and mechanisms of moon dust toxicity.