UVA can cause oxidative stress and photoaging of cells. We established a UVA-induced oxidative stress model of human fibroblasts and focused on the antioxidant and anti-photoaging ability of Lactobacillus plantarum fermented Rhodiola rosea. Compared with the unfermented Rhodiola rosea, Lactobacillus plantarum fermented Rhodiola rosea has better DPPH free radical and hydroxyl free radical scavenging ability, significantly reduces the content of reactive oxygen species (ROS), and improves the antioxidant level. Further studies have shown that the Lactobacillus plantarum fermented Rhodiola rosea can activate the Nrf2/Keap1 signaling pathway and up-regulate heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), catalase (CAT) and glutathione Peptide peroxidase (GSH-Px), and protect fibroblasts from oxidative stress caused by UVA. On the other hand, Lactobacillus plantarum fermented Rhodiola rosea significantly reduces the activity of metalloproteinases in the cell, thereby increasing the collagen and elastin in the cell, alleviating the photoaging caused by UVA. Finally, we concluded that the antioxidant capacity and anti-photoaging ability of Lactobacillus plantarum fermented Rhodiola rosea are better than that of unfermented Rhodiola rosea.

Acne is a chronic inflammatory skin disease with a recurring nature that seriously impacts patients’ quality of life. Currently, antibiotic resistance has made it less effective in treating acne. However, Paris polyphylla (P. polyphylla) is a valuable medicinal plant with a wide range of chemical components. Of these, P. polyphylla saponins modulate the effects in vivo and in vitro through antibacterial, anti-inflammatory, immunomodulatory, and antioxidant effects. Acne is primarily associated with inflammatory reactions, abnormal sebum function, micro-ecological disorders, hair follicle hyperkeratosis, and, in some patients, immune function. Therefore, the role of P. polyphylla saponins and their values in treating acne is worthy of investigation. Overall, this review first describes the distribution and characteristics of P. polyphylla and the pathogenesis of acne. Then, the potential mechanisms of P. polyphylla saponins in treating acne are listed in detail (reduction in the inflammatory response, antibacterial action, modulation of immune response and antioxidant effects, etc.). In addition, a brief description of the chemical composition of P. polyphylla saponins and its available extraction methods are described. We hope this review can serve as a quick and detailed reference for future studies on their potential acne treatment.

Ectoin is an amino acid derivative that can create a balance between the osmotic pressure of cells and can protect enzymes, DNA proteins, and nucleic acids under extreme conditions. Ectoin has also been reported to slow skin aging. However, there are few reports on the protective effect of Ectoin on oxidative damage, especially on the regulation of PI3K/AKT-pathway-related genes at the mRNA level. UVA-induced oxidative stress injury and H₂O₂-induced oxidative stress injury are two common oxidative stress injury models. Skin fibroblasts produce a large number of ROS following excessive UV radiation or oxidative stimulation by H₂O₂, which further inhibits cell proliferation and causes cell apoptosis. In this study, UVA- and H₂O₂-induced oxidation models of human skin fibroblasts were established separately to investigate the protective effect of Ectoin. Further studies on the mechanisms involved, for example, the expression levels of genes associated with the PI3K/AKT signaling pathway and levels of antioxidant enzymes in cells, were determined. We found that Ectoin upregulated genes associated with the PI3K/AKT signaling pathway, including COL1A1, COL1A2, FN1, IGF2, NR4A1, and PIK3R1, but decreased intracellular ROS levels and malondialdehyde (MDA), while increasing the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). In conclusion, our results indicate that Ectoin exerts protective properties by the upregulated genes COL1A1, COL1A2, FN1, IGF2, NR4A1, and PIK3R1 and upregulating antioxidative enzyme levels.

Treatment of epithelial ovarian cancer (EOC) is a challenge because it still leads to unsatisfactory clinical prognosis. This is due to the toxicity and poor targeting of chemotherapeutic agents, as well as metastasis of the tumor. In this study, we designed a targeted liposome with nanostructures to overcome these problems. In the liposomes, epirubicin and curcumin were encapsulated to achieve their synergistic antitumor efficacy, while Epi-1 was modified on the liposomal surface to target epithelial cell adhesion molecule (EpCAM). Epi-1, a macrocyclic peptide, exhibits active targeting for enhanced cellular uptake and potent cytotoxicity against tumor cells. The encapsulation of epirubicin and curcumin synergistically inhibited the formation of neovascularization and vasculogenic mimicry (VM) channels, thereby suppressing tumor metastasis on SKOV3 cells. The dual drug loaded Epi-1-liposomes also induced apoptosis and downregulated metastasis-related proteins for effective antitumor in vitro. In vivo studies showed that dual drug loaded Epi-1-liposomes prolonged circulation time in the blood and increased the selective accumulation of drug at the tumor site. H&E staining and immunohistochemistry with Ki-67 also showed that targeted liposomes elevated antitumor activity. Also, targeted liposomes downregulated angiogenesis-related proteins to inhibit angiogenesis and thus tumor metastasis. In conclusion, the production of dual drug loaded Epi-1-liposomes is an effective strategy for the treatment of EOC.

Purpose We aimed to find active substances to help relieve the symptoms caused by increased photosensitivity after alpha hydroxy acid (AHA) peeling. Methods: A questionnaire survey was provided to 66 patients who received AHA peeling therapy to understand if increased photosensitivity existed and its specific symptoms. We verified increased photosensitivity after AHA peeling by monitoring cell viability to detect the combined toxicity of glycolic acid (GA) and UVB in HaCaT cells. The ELISA method was used to determine the expression of KLK7, FLG, IL-1β, and IL-8 to correlate damage to the skin barrier and inflammation induced by GA and UVB and the relieving effects of Portulaca oleracea extract. Results: Our survey results showed that 6.06% of people were more sensitive to sunlight after AHA peeling than before. Experiments at the cellular level showed that UVB induced cytotoxicity on HaCaT cells pre-treated with GA. Combined exposure of GA and UVB induced up-regulation of KLK7 and down-regulation of FLG and increased inflammatory cytokines of IL-1β and IL-8. Portulaca oleracea extract inhibited the reduction of FLG and increased KLK7, IL-1β, and IL-8 expression caused by combined exposure. Conclusions: Our study found that combined exposure to GA and UV disrupted the skin barrier and induced significant inflammation. These results provided a theoretical basis for increased photosensitivity after chemical peeling. Portulaca oleracea extract ameliorated GA and UVB-induced impaired skin barrier function and inflammation in HaCaT cells and may have the potential to relieve photosensitivity after AHA peeling.