Centella asiatica (C. asiatica) is a pharmacological plant in South Asia. It has been demonstrated that C. asiatica extracts containing various pentacyclic triterpenes exert healing effects, especially wound healing and collagen synthesis in skin. However, there are few studies on the effect of C. asiatica extracts on stress-induced premature senescence (SIPS). To determine whether H(2) O(2) -induced senescence is affected by C. asiatica extracts, we performed senescence analysis on cultured human dermal fibroblasts (HDFs). We also analysed whole gene expression level using microarrays and showed that 39 mRNAs are differentially expressed in H(2) O(2) -induced HDFs with and without treatment with C. asiatica extracts. These genes regulate apoptosis, gene silencing, cell growth, transcription, senescence, DNA replication and the spindle checkpoint. Differential expression of FOXM1, E2F2, MCM2, GDF15 and BHLHB2 was confirmed using semi-quantitative PCR. In addition, C. asiatica extracts rescued the H(2) O(2) -induced repression of replication in HDFs. Therefore, the findings presented here suggest that C. asiatica extracts might regulate SIPS by preventing repression of DNA replication and mitosis-related gene expression.
"The gel layer may remain in place for up to 6 h. PP contains extracts of three herbs: Centella asiatica, Echinacea purpurea and Sambucus nigra which have been shown to present healing effects, especially wound healing and collagen synthesis in skin (Kim et al. 2011), to positively affect the expression of genes involved in angiogene- sis and the remodelling of extracellular matrix (Coldren et al. 2003) and be effective in reducing gingival inflammation (Sastravaha et al. 2003, 2005, Harokopakis et al. 2006). Centella Asiatica extract presents a multiplicity of actions associated to six important mechanisms: oedema and capillary filtration control ; strong antioxidant power, effective on several forms of oxidative stress associated to inflammation or infections and synergic with other antioxidant products; an antiinflammatory action; a modulation of the collagen production avoiding slower scarring or faster, hyperthrophic scarring and cheloids; a modulating action of local growth factors; a modulation of angiogenesis (Belcaro et al. 2011). "
[Show abstract][Hide abstract] ABSTRACT: AimThe present study evaluated the effects of a topical herbal patch (PerioPatch®) for gingival wound healing in a rat model.Materials and MethodsA mid-crestal incision was performed on each side of the edentulous anterior maxilla in 48, six-month-old, Wistar rats. Full thickness flaps were raised, repositioned and sutured. Four experimental groups were established: herbal patch, placebo patch, no patch and no patch and no surgery. Patches were placed immediately after surgery and replaced every 12 hours for the following 3 days. Half of the animals were sacrificed after 5 and the remaining ones after 12 days. Tissue blocks were retrieved and processed for histological and immunohistochemical evaluation. Epithelial gap, collagen contents, amount of macrophages, cellular proliferation, and vascular contents were evaluated in the central incision area. Statistical analysis consisted of 2-way ANOVA.ResultsThe herbal patch group presented the smallest epithelial gap at 12 days, the highest collagen content both at 5 and 12 days, a larger number of proliferating cells at day 5 and more numerous blood vessels at day 12. Macrophage number was similar in all groups.Conclusion
Herbal patch improved wound healing in this animal model.This article is protected by copyright. All rights reserved.
"Intercellular ROS levels were measured using 2′,7′-dichlorofluorescein diacetate (DCF-DA) (Sigma-Aldrich) as previously described (17). nHDPs were plated onto 60-mm tissue culture dishes at a density of 2x106 cells/plate. "
[Show abstract][Hide abstract] ABSTRACT: Ultraviolet (UV) radiation impairs intracellular functions by directly damaging DNA and by indirectly generating reactive oxygen species (ROS), which induce cell cycle arrest and apoptosis. UV radiation can also alter gene expression profiles, including those of mRNA and microRNA (miRNA). The effects of UV radiation on cellular functions and gene expression have been widely documented in human skin cells such as keratinocytes, melanocytes and dermal fibroblasts, but the effect it has on other types of skin cell such as dermal papilla cells, which are crucial in the induction of hair follicle growth, remains unknown. In the current study, the effect of UV radiation on physiological changes and miRNA‑based expression profiles in normal human dermal papilla cells (nHDPs) was investigated. UVB radiation of ≥50 mJ/cm2 displayed high cytotoxicity and apoptosis in a dose‑dependent manner. In addition, ROS generation was exhibited in UVB‑irradiated nHDPs. Furthermore, using miRNA microarray analysis, it was demonstrated that the expression profiles of 42 miRNAs in UVB‑irradiated nHDPs were significantly altered compared with those in the controls (35 upregulated and 7 downregulated). The biological functions of the differentially expressed miRNAs were studied with gene ontology analysis to identify their putative target mRNAs, and were demonstrated to be involved in cell survival‑ and death‑related functions. Overall, the results of the present study provide evidence that miRNA‑based cellular mechanisms may be involved in the UVB‑induced cellular response in nHDPs.
Molecular Medicine Reports 07/2014; 10(4). DOI:10.3892/mmr.2014.2418 · 1.55 Impact Factor
"Previous studies indicate that there are similar results when HDFs and NIH 3T3 cells under the same stimulates such as MEK inhibitor PD98059 and IL-1 suppress basal and TGF-binduced CTGF mRNA and protein expression (Zhao et al., 2004; Nowinski et al., 2010). Recent studies have demonstrated that Centella asiatica extracts regulates HDFs senescence induced by hydrogen peroxide partly through promoting FOXM1 expression (Kim et al., 2011). FoxM1 counteracts oxidative stress-induced NIH 3T3 cells senescence via up-regulating c-Myc expression, resulting in suppressing p21 expression (Li et al., 2008). "
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