In Vitro Inhibition of Cell Growth, Collagen Synthesis, and Prolyl Hydroxylase Activity by Triamcinolone Acetonide

Bj, McCoy; Rf, Diegelmann; Ik, Cohen

doi:10.3181/00379727-163-40750

Cited by 123 publications

(77 citation statements)

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“…The corticosteroid inhibits alpha2-macroglobulin, which in turn inhibits collagenase. Once this pathway is blocked, collagenase is elaborated, thus enabling collagen degeneration 29 .…”

Section: Discussionmentioning

confidence: 99%

Surgery and Perioperative Intralesional Corticosteroid Injection for Treating Earlobe Keloids: A Korean Experience

et al. 2009

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Background:The aesthetic implications of ear keloids, which affect people of all races, are serious and the treatment of earlobe keloids is known to be difficult. The high rate of recurrence following excision alone has led to investigating various types of adjuvant therapy, including intralesional corticosteroid injection. Objective: We evaluated the efficacy of excision combined with perioperative intralesional triamcinolone acetonide injection for treating earlobe keloids of Korean patients. Methods: From 1997 to 2006, eighteen keloids on the earlobes of fifteen Korean patients were treated. The patient age ranged from 15 to 32 years (mean age: 24 years). All the patients were female and the keloids occurred after ear piercing. Preoperative intralesional triamcinolone acetonide (TA) injection was administered twice at a 1-month interval. Postoperative intralesional TA injections were given every 1 month for several months, depending on the patient's clinical progress. Results: The follow-up period ranged from 4 to 42 months (mean: 18.5 months). After the surgery, TA intralesional injections were given 2 to 13 times (mean: 5.2 times). Of the treated keloids, eleven showed good results (61.1%) and three recurred (16.6%). No complications from the TA intralesional injection were observed. Conclusion: Among the various treatments for earlobe keloids, we suggest that excision with corticosteroid intralesional injection can be used as the first line therapy when considering its effect and economic advantage. (Ann Dermatol 21(3) 221∼225, 2009)

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“…The corticosteroid inhibits alpha2-macroglobulin, which in turn inhibits collagenase. Once this pathway is blocked, collagenase is elaborated, thus enabling collagen degeneration 29 .…”

Section: Discussionmentioning

confidence: 99%

Surgery and Perioperative Intralesional Corticosteroid Injection for Treating Earlobe Keloids: A Korean Experience

et al. 2009

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“…[7][8][9][10] Steroid injections are often used to treat unresponsive scars. [11][12][13][14] Silicone gel was first used underneath pressure garments to achieve a better fit and was fortuitously noted to have a beneficial effect on hypertrophic burn scars. 15 Quinn et al 16 confirmed the beneficial effects in a larger uncontrolled study.…”

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confidence: 99%

Silicone occlusive treatment of hypertrophic scar in the rabbit model

Saulis

Chao

Telser

et al. 2002

Aesthetic Surgery Journal

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“…Tranilast specifically suppresses the collagen synthesis rather than the cell proliferation by cultured fibroblasts derived from human keloid tissues (7). On the other hand, triamcinolone, a synthetic steroid, can suppress the cell proliferation and collagen synthesis of fibro blasts (8,9). For these reasons, attention has been paid to the fact that the inhibitory mechanisms of tranilast differs from that of triamcinolone.…”

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confidence: 99%

The Mechanism Involved in the Inhibitory Action of Tranilast on Collagen Biosynthesis of Keloid Fibroblasts.

et al. 1992

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ABSTRACT-Tranilast, an anti-allergic drug inhibiting the release of substances such as histamine and prostaglandins from mast cells, was previously reported to suppress collagen synthesis of fibroblasts de rived from keloid tissues. However, the inhibitory mechanism on collagen synthesis is unknown. We studied its inhibitory mechanism on collagen synthesis by culturing fibroblasts from keloid and hyper trophic scar tissues of humans. Collagen synthesis of fibroblasts from keloid and hypertrophic scar tis sue is greater than that from healthy human skin. Tranilast (3 -100 ,u M) did not inhibit prolyl hydrox ylase (the rate-limiting enzyme in collagen synthesis) activity. Tranilast (3 300 ,uM) suppressed the col lagen synthesis of fibroblasts from keloid and hypertrophic scar tissue but not healthy skin fibro blasts. Tranilast (30 300 ,u M) inhibited the release of transforming growth factor (TGF)-,81 from keloid fibroblasts, which enhances the collagen synthesis of keloid fibroblasts. Anti-TGF-,81 antibody (50,ul/ml) inhibited the collagen synthesis, although diphenhydramine (10 ,aM) and indomethacin (10 ,uM) did not show any inhibition. These results suggest that tranilast inhibits collagen synthesis of fibroblasts from keloid and hypertrophic scar tissue through suppressing the release of TGF-,8, from the fibroblasts themselves.Keywords: Tranilast, Collagen synthesis, Keloid fibroblast, Transforming growth factor (TGF)-,81, Cytokine Hypertrophic scar and keloid are clinically intractable diseases that cause disfigurement, itching and pain. The etiology of these diseases is not known with certainty. During the granulation period in the process of healing at injured sites such as surgical wounds, bums and so on, abnormal proliferation of fibroblasts and production of collagen result in keloids with the accumulation of excessive collagen (1 3).It is well-known that tranilast is an useful drug for improving bronchial asthma, atopic dermatitis and aller gic rhinitis. Several reports have shown that tranilast can prevent or act to improve keloid and hypertrophic scars (4, 5). Tranilast decreases the weight of granula tion and inhibits the collagen synthesis by human keloid tissues transplanted into the backs of mice and by carrageenin-induced granulation-tissues in rats (6-8). Tranilast specifically suppresses the collagen synthesis rather than the cell proliferation by cultured fibroblasts derived from human keloid tissues (7). On the other hand, triamcinolone, a synthetic steroid, can suppress the cell proliferation and collagen synthesis of fibro blasts (8,9). For these reasons, attention has been paid to the fact that the inhibitory mechanisms of tranilast differs from that of triamcinolone. In general, the in hibition of protein synthesis by corticosteroids has been considered the reason for decreased collagen synthesis in dermal tissue. However, the precise mechanism for the action of tranilast on the collagen synthesis is yet unknown.In the present study, we studied the suppressive mechanism of tranilast on th...

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In Vitro Inhibition of Cell Growth, Collagen Synthesis, and Prolyl Hydroxylase Activity by Triamcinolone Acetonide

Cited by 123 publications

References 0 publications

Surgery and Perioperative Intralesional Corticosteroid Injection for Treating Earlobe Keloids: A Korean Experience

Surgery and Perioperative Intralesional Corticosteroid Injection for Treating Earlobe Keloids: A Korean Experience

Silicone occlusive treatment of hypertrophic scar in the rabbit model

The Mechanism Involved in the Inhibitory Action of Tranilast on Collagen Biosynthesis of Keloid Fibroblasts.

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