Oleanolic acid inhibits hypertrophic scarring in the rabbit ear model

Wei, Yan-Jie; Yan, Xue; Ma, Li; Wu, Jian; Zhang, Hong; Qin, Lu‐Ping

doi:10.1111/j.1365-2230.2010.04012.x

Cited by 15 publications

(13 citation statements)

References 13 publications

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“…We observed further the effects of OA on scar-related parameters in the rabbit ear scar model. The results suggest that OA has significant preventive and therapeutic effects on hypertrophic scars (Wei et al, 2011;Zhang et al, 2012a). Subsequently, we evaluated any possible toxicity of OA by an acute toxicity test.…”

Section: Introductionmentioning

confidence: 99%

Triggering of p38 MAPK and JNK Signaling is Important for Oleanolic Acid‐Induced Apoptosis via the Mitochondrial Death Pathway in Hypertrophic Scar Fibroblasts

Chen

Zhang

et al. 2014

Phytotherapy Research

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Hypertrophic scarring is characterized by collagen overproduction and excessive deposition of extracellular matrix. No consensus arises currently about the best therapeutics to produce complete and permanent improvement of scars with few side effects. In the present study, the mechanism of oleanolic acid (OA)-induced apoptosis in hypertrophic scar fibroblasts (HSFs) was investigated for the first time. OA activated the protein phosphorylation of p38 MAPK and JNK but not ERK. OA did not antagonize the inhibitory effects of SB203580 on p38 MAPK pathway activity but sharply enhanced JNK phosphorylation when HSFs were pretreated with SB203580. Similarly, the inhibition of JNK signal pathway activation by pretreatment with SP600125 facilitated the protein phosphorylation of p38 MAPK caused by OA. Inhibition of p38 MAPK and/or JNK by inhibitors significantly enhanced cell viability and OA only partially depressed the increased cell viability. Moreover, OA increased Bax translocation, MMP loss, mitochondrial cytochrome c and AIF release, Bax and caspase-3 protein expression and the ratio of Bax to Bcl-2, decreased Bcl-2 protein expression, and elevated the mRNA expression of Apaf-1, caspase-9, and capase-3. These results suggest that OA elicits apoptosis through triggering of p38 MAPK and JNK signaling and activation of the mitochondrial death pathway. OA might be a good and useful natural drug against hypertrophic scars.

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Section: Introductionmentioning

confidence: 99%

Triggering of p38 MAPK and JNK Signaling is Important for Oleanolic Acid‐Induced Apoptosis via the Mitochondrial Death Pathway in Hypertrophic Scar Fibroblasts

Chen

Zhang

et al. 2014

Phytotherapy Research

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“…[10] C. ternatea extract and fractions were diluted at different concentrations and screened in triplicate ( n = 3) for the inhibitory activities on elastase, hyaluronidase, and MMP-1 compared with standard oleanolic acid, which is a pentacyclic triterpene found in several botanical extracts and is also responsible to inhibit the dermal enzymatic process in skin wounds. [1112] The inhibition of each enzyme due to the test substance was calculated. The hyaluronidase, elastase, and MMP-1 inhibitory activity of CTMeOH extract and the CTEA fraction were found to be more than oleanolic acid.…”

Section: Discussionmentioning

confidence: 99%

Standardized Clitoria ternatea leaf extract as hyaluronidase, elastase and matrix-metalloproteinase-1 inhibitor

et al. 2012

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Aim:Plant Clitoria ternatea L. is claimed to possess a wide range of activities including antiinflammatory, local anesthetic and antidiabetic effect, etc. The aim of the present study was to evaluate the wound healing potential of standardized C. ternatea leaf extract in terms of different enzymatic models, which are mostly associated with skin wound.Materials and Methods:The methanol extract and fractions were screened for its hyaluronidase, elastase, and matrix metalloproteinase-1 (MMP-1) inhibitory activity compared with standard oleanolic acid. The activity was rationalized through reverse phase high performance liquid chromatography (RP-HPLC) standardization of the extract and fractions with respect to its isolated biomarker taraxerol (yield 5.27% w/w).Results:The extract showed significant (P < 0.001) hyaluronidase (IC50 18.08 ± 0.46 μg/ ml) and MMP-1 (P < 0.05) inhibition, but the elastase inhibition was insignificant (IC50 42.68 ± 0.46 μg/ml). Among the fractions, ethyl acetate fraction showed significant (P < 0.001) inhibition of hyaluronidase (IC50 28.01 ± 0.48 μg/ml) and MMP-1 (P < 0.01). The HPLC analysis revealed that the extract and the ethyl acetate fraction are enriched with taraxerol (5.32% w/w and 4.55% w/w, respectively).Conclusions:The experiment validated the traditional uses of C. ternatea and may be recommended for use in the treatment of different types of skin wounds, where taraxerol may be a responsible biomarker.

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“…57 Studies show that after OA treatment, the level of MMP-1 and MMP-2 was increased in the rabbit HSs model and the HS was suppressed significantly. 58,59 Additionally, compared with the higher collagen-III in normal skin, there is a high ratio of collagen-I to III in HSs, which could be reversed by OA.…”

Section: Traditional Plant-based Medicine and Productsmentioning

confidence: 99%

Biological approaches for hypertrophic scars

Zhong

2019

International Wound Journal

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Scar formation is usually the pathological consequence of skin trauma. And hypertrophic scars (HSs) frequently occur in people after being injured deeply. HSs are unusually considered as the result of tissue contraction and excessive extracellular matrix component deposition. Myofibroblasts, as the effector cells, mainly differentiated from fibroblasts, play the crucial role in the pathophysiology of HSs. A number of growth factors, inflammatory cytokines involved in the process of HS occurrence. Currently, with in‐depth exploration and clinical research of HSs, various creative and effective treatments budded. In here, we summarize the progress in the molecular mechanism of HSs, and review the available biotherapeutic methods for their pathophysiological characteristics. Additionally, we further prospected that the comprehensive therapy may be more suitable for HS treatment.

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Oleanolic acid inhibits hypertrophic scarring in the rabbit ear model

Abstract: OA suppresses hypertrophic scarring in the rabbit ear model and may be an effective cure for human hypertrophic scarring.

Cited by 15 publications

References 13 publications

Triggering of p38 MAPK and JNK Signaling is Important for Oleanolic Acid‐Induced Apoptosis via the Mitochondrial Death Pathway in Hypertrophic Scar Fibroblasts

Triggering of p38 MAPK and JNK Signaling is Important for Oleanolic Acid‐Induced Apoptosis via the Mitochondrial Death Pathway in Hypertrophic Scar Fibroblasts

Standardized Clitoria ternatea leaf extract as hyaluronidase, elastase and matrix-metalloproteinase-1 inhibitor

Biological approaches for hypertrophic scars

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