Introduction: Inflammation generally refers to the body’s defensive response to stimuli, and skin inflammation is still one of the major problems that affect human physical and mental health. While current pharmacological treatments are reported to have cytotoxicity and various side effects, herbal medicines with few side effects and low cytotoxicity are considered as alternative therapeutic approaches. Methods: In order to investigate anti-inflammatory effects and mechanisms of ALOE, the potential cytotoxicity of A. vera extracts (ALOE) was determined in vitro at first. The production of the pro-inflammatory proteins (ie, IL-6, TNF-α) in lipopolysaccharides (LPS) and ultraviolet A (UVA)-stimulated HaCaT and RAW264.7 cells were then treated with ALOE to test its inhibitory effects using enzyme-linked immunosorbent assay (ELISA). To further explore the anti-inflammatory mechanisms of ALOE, quantitative Polymerase Chain Reaction (qPCR) was used to analyze the mRNA expression of inflammatory genes iNOS, COX-2 and NO production. For NF-κB and MAPK signaling pathways analysis, Western blotting and nuclear fluorescence staining were used to evaluate the expression of key factors. Results: ALOE did not exhibit obvious cytotoxicity (0– 3 mg/mL) in vitro. ALOE was able to inhibit the expression of pro-inflammatory cytokines IL-6, TNF-α and functioned more prominently in LPS-induced model. ALOE could also suppress the mRNA expression of LPS-induced iNOS and COX-2 and further down-regulate NO level. Furthermore, ALOE reduced the protein expression of P65 in NF-κB signaling pathway and suppressed LPS-induced activation of ERK and JNK, instead of p38 MAPK pathway. Conclusion: Taken together, these results demonstrated that ALOE is a potential treatment in suppressing LPS-stimulated inflammation reactions targeting NF-κB, JNK and ERK signaling pathways. The anti-inflammatory effects of ALOE indicated that it has the potential to become an effective cosmetic ingredient.

Background: Centella asiatica (CA) has been used to address cancer for centuries in traditional Chinese medicine (TCM). Previous studies demonstrated its anti-angiogenesis efficacy, but the underlying mechanism of its action remains to be further clarified. This study aims to investigate the underlying mechanisms of CA and its triterpenes in anti-angiogenesis for cancer therapeutics through network pharmacology and experimental validation. Methods: Cytoscape was used to construct a network of compound–disease targets and protein–protein interactions (PPIs) from which core targets were identified. GO and KEGG analyses were performed using Metascape, and the AutoDock-Vina program was used to realize molecular docking for further verification. Then, VEGF165 was employed to establish an induced angiogenesis model. The anti-angiogenic effects of CA were evaluated through assays measuring cell proliferation, migration, and tubular structure formation. Results: Twenty-five active ingredients in CA had potential targets for anti-angiogenesis including madecassoside, asiaticoside, madecassic acid, asiatic acid, and asiaticoside B. In total, 138 potential targets for CA were identified, with 19 core targets, including STAT3, SRC, MAPK1, and AKT1. A KEGG analysis showed that CA is implicated in cancer-related pathways, specifically PD-1 and AGE-RAGE. Molecular docking verified that the active components of CA have good binding energy with the first four important targets of angiogenesis. In experimental validation, the extracts and triterpenes of CA improved VEGF165-induced angiogenesis by reducing the proliferation, migration, and tube formation of human umbilical vein endothelial cells (HUVECs). Conclusions: Our results initially demonstrate the effective components and great anti-angiogenic activity of CA. Evidence of the satisfactory anti-angiogenic action of the extracts and triterpenes from CA was verified, suggesting CA’s significant potential as a prospective agent for the therapy of cancer.

Acne vulgaris represents a chronic inflammatory condition, the pathogenesis of which is closely associated with the altered skin microbiome. Recent studies have implicated a profound role of Gram‐negative bacteria in acne development, but there is a lack of antiacne agents targeting these bacteria. Polyphyllins are major components of Rhizoma Paridis with great anti‐inflammatory potential. In this study, we aimed to evaluate the antiacne effects and the underlying mechanisms of PPH and a PPH‐enriched Rhizoma Paridis extract (RPE) in treating the Gram‐negative bacteria‐induced acne. PPH and RPE treatments significantly suppressed the mRNA and protein expressions of interleukin (IL)‐1β and IL‐6 in lipopolysaccharide (LPS)‐induced RAW 264.7 and HaCaT cells, along with the intracellular reactive oxygen species (ROS) generation. Furthermore, PPH and RPE inhibited the nuclear translocation of nuclear factor kappa‐B (NF‐κB) P65 in LPS‐induced RAW 264.7 cells. Based on molecular docking, PPH could bind to kelch‐like ECH‐associated protein 1 (KEAP1) protein. PPH and RPE treatments could activate nuclear factor erythroid 2‐related factor 2 (NRF2) and upregulate haem oxygenase‐1 (HO‐1). Moreover, RPE suppressed the mitogen‐activated protein kinase (MAPK) pathway. Therefore, PPH‐enriched RPE showed anti‐inflammatory and antioxidative effects in vitro, which is promising for alternative antiacne therapeutic.

Yunnan Baiyao is a well-known traditional Chinese medicine that can be formulated into a powder or capsule form. The mechanism by which it exerts its anti-inflammation effect, which is used in skin care products, needs to be further explored. In this study, we established the Staphylococcus aureus-induced mouse skin inflammatory model to investigate the effects of Yunnan Baiyao by the method of RNA-sequencing technology. The mice were randomly assigned to three groups, and those were control, model, and the Yunnan Baiyao-treated (YNtreated) group. Key genes and pathways were identified using bioinformatics analyses. In the study, we obtained 1,053 differentially expressed genes (DEGs) induced by Yunnan Baiyao. The 233 upregulated genes were enriched in 32 GO terms and 5 KEGG pathways, focused on the items, such as wound healing, cell metabolism, and proliferation, indicating the accelerating effects of Yunnan Baiyao on these aspects. The 820 downregulated genes were enriched mainly in the items, including the regulation of inflammation factor production, immune responses, and regulation of structure dermal components. Besides, Yunnan Baiyao reversed the expressions of 277 (201 decreased and 76 increased DEGs, respectively) induced by S. aureus. Ten key regulatory nodes (MMP2, PLK1, CCNB1, TLR4, CDK1, CCNA2, CDC25C, PDGFRA, MYOC, and KNG1) were identified by the construction of the protein interaction network, half of which were related to cell proliferation. VAV1 was another hub node that was affected by Yunnan Baiyao (Top 20). In the study, VAV1 and TLR4 can be considered key module genes in inflammation regulation. In conclusion, this study found that Yunnan Baiyao can significantly relieve inflammatory symptoms by regulating genes and pathways involved in the regulation of inflammation and immune response and also helped to deepen our understanding of the associated molecular mechanisms.

Skin hyperpigmentation is a worldwide condition associated with augmented melanogenesis. However, conventional therapies often entail various adverse effects. Here, we explore the safety range and depigmentary effects of polysaccharides extract of Tricholoma matsutake (PETM) in an in vitro model and further evaluated its efficacy at the clinical level. An induced-melanogenesis model was established by treating B16–F10 melanoma cells with 8-methoxypsoralen (8-MOP). Effects of PETM on cell viability and melanin content were examined and compared to a commonly used depigmentary agent, α-arbutin. Expressions of key melanogenic factors and upstream signaling pathway were analysed by quantitative PCR and western blot. Moreover, a placebo-controlled clinical study involving Chinese females with skin hyperpigmentation was conducted to measure the efficacy of PETM on improving facial pigmented spots, melanin index, and individual typology angle (ITA°). Results demonstrated that PETM (up to 0.5 mg/mL) had little effect on the viability and motility of B16–F10 cells. Notably, it significantly suppressed the melanin content and expressions of key melanogenic factors induced by 8-MOP in B16–F10 melanoma cells. Western blotting results revealed that PETM inhibited melanogenesis by inactivating c-Jun N-terminal kinase (JNK), and this inhibitory role could be rescued by JNK agonist treatment. Clinical findings showed that PETM treatment resulted in a significant reduction of facial hyperpigmented spot, decreased melanin index, and improved ITA° value compared to the placebo-control group. In conclusion, these in vitro and clinical evidence demonstrated the safety and depigmentary efficacy of PETM, a novel polysaccharide agent. The distinct mechanism of action of PETM on melanogenic signaling pathway positions it as a promising agent for developing alternative therapies.