Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2010
[Effects of radix astragali on expression of transforming growth factor β 1 and Smad 3 signal pathway in hypertrophic scar of rabbit].
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zhang Yan, Qiu Lin, Li Ming-yong
Аннотация
OBJECTIVE: To observe the effects of radix astragali on expression of TGF-β₁ and Smad 3 signal pathway in hypertrophic scar of rabbits, and to analyze its therapeutic effect and mechanism on hypertrophic scar.
METHODS: Twenty healthy adult Japanese big ear rabbits were inflicted with 4 full-thickness skin defects on ventral side of each ear, which formed scar later. Rabbits were divided into 5 groups: 1.00, 0.50, 0.25 g/mL radix astragali treatment groups [injected with radix astragali on post injury day (PID) 21, 25, 32, and 36 respectively], physiological saline group (PS, injected with 0.2 mL physiological saline in the same volume at the same time points as above groups), and blank control group (BC, without treatment) according to the random number table, with 32 scars in each group. Another 4 rabbits were enrolled as normal control group (NC). Structural changes of hypertrophic scar was observed with HE and Masson staining. Thickness and hardness of hypertrophic scar on PID 32 and 43 were respectively examined by chromoscope ultrasonic diagnostic equipment and hardness tester. Protein and mRNA expression of TGF-β₁ and Smad 3 in hypertrophic scar was respectively detected with RT-PCR and immunohistochemical analysis. Data were processed with t test and one-way analysis of variance.
RESULTS: Compared with that in PS and BC groups, dermis of hypertrophic scar became thinner in radix astragali treatment groups on PID 32, 43, with fibroblasts and collagenous fibers arranged regularly on PID 43. Thickness and hardness of hypertrophic scar, levels of mRNA and protein of TGF-β₁ and Smad 3 decreased along with the increase in radix astragali concentration. Compared with those in PS group, levels of mRNA of TGF-β₁ and Smad 3 in 1.00 g/mL radix astragali treatment group on PID 32 decreased 26.1% and 28.2%. Protein levels of TGF-β₁ and Smad 3 in 1.00 g/mL radix astragali treatment group were 3.15 ± 0.80 and 4.72 ± 1.06, which were obviously lower than those in PS group (6.06 ± 0.85, 8.04 ± 0.63, with F value respectively 27.230 and 33.525, P < 0.05 or P < 0.01). There was significant statistical difference in all measurement indices except for mRNA of TGF-β₁ and Smad 3 among radix astragali treatment groups on PID 32 and 43 [with t values respectively 3.593-4.814 (thickness), 4.051-5.811 (hardness), 2.976-5.986 (TGF-β₁ protein), and 2.742-4.630 (Smad 3 protein), P < 0.05 or P < 0.01].
CONCLUSIONS: Radix astragali injection inhibits fibroblast proliferation in hypertrophic scars through down-regulating mRNA expression and protein synthesis of TGF-β₁ and Smad 3, thus inhibits hypertrophic scars formation. Its inhibition effect is drug concentration and duration dependent. The drug may be considered as a potential agent to prevent hypertrophic scar.
METHODS: Twenty healthy adult Japanese big ear rabbits were inflicted with 4 full-thickness skin defects on ventral side of each ear, which formed scar later. Rabbits were divided into 5 groups: 1.00, 0.50, 0.25 g/mL radix astragali treatment groups [injected with radix astragali on post injury day (PID) 21, 25, 32, and 36 respectively], physiological saline group (PS, injected with 0.2 mL physiological saline in the same volume at the same time points as above groups), and blank control group (BC, without treatment) according to the random number table, with 32 scars in each group. Another 4 rabbits were enrolled as normal control group (NC). Structural changes of hypertrophic scar was observed with HE and Masson staining. Thickness and hardness of hypertrophic scar on PID 32 and 43 were respectively examined by chromoscope ultrasonic diagnostic equipment and hardness tester. Protein and mRNA expression of TGF-β₁ and Smad 3 in hypertrophic scar was respectively detected with RT-PCR and immunohistochemical analysis. Data were processed with t test and one-way analysis of variance.
RESULTS: Compared with that in PS and BC groups, dermis of hypertrophic scar became thinner in radix astragali treatment groups on PID 32, 43, with fibroblasts and collagenous fibers arranged regularly on PID 43. Thickness and hardness of hypertrophic scar, levels of mRNA and protein of TGF-β₁ and Smad 3 decreased along with the increase in radix astragali concentration. Compared with those in PS group, levels of mRNA of TGF-β₁ and Smad 3 in 1.00 g/mL radix astragali treatment group on PID 32 decreased 26.1% and 28.2%. Protein levels of TGF-β₁ and Smad 3 in 1.00 g/mL radix astragali treatment group were 3.15 ± 0.80 and 4.72 ± 1.06, which were obviously lower than those in PS group (6.06 ± 0.85, 8.04 ± 0.63, with F value respectively 27.230 and 33.525, P < 0.05 or P < 0.01). There was significant statistical difference in all measurement indices except for mRNA of TGF-β₁ and Smad 3 among radix astragali treatment groups on PID 32 and 43 [with t values respectively 3.593-4.814 (thickness), 4.051-5.811 (hardness), 2.976-5.986 (TGF-β₁ protein), and 2.742-4.630 (Smad 3 protein), P < 0.05 or P < 0.01].
CONCLUSIONS: Radix astragali injection inhibits fibroblast proliferation in hypertrophic scars through down-regulating mRNA expression and protein synthesis of TGF-β₁ and Smad 3, thus inhibits hypertrophic scars formation. Its inhibition effect is drug concentration and duration dependent. The drug may be considered as a potential agent to prevent hypertrophic scar.