A Study on the Relationship between the Expression of Caspase-3 and Toll-like Receptor 4 and the Injury Time in Incised Rat Skin Healing_West China Medical Journal

Authors：

 ZHANGDong-xue ¹ , GONGDao-yin ² , DAIHao ¹ , YUYou-jia ¹ , LUMei-gui ¹ , CAOYong ¹ ,  HUANGFei-jun ¹

1. Department of Forensic Pathology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, P. R. China;
2. Department of Pathology, West China School of Preclinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611333, P. R. China;

Corresponding?author：

HUANGFei-jun, Email: 787633295@qq.com

Keywords：

Forensic pathology; Wound time estimation; Incised skin injury; Immunohistochemistry; Caspase-3; Toll-like receptor 4; Rats

DOI：

10.7507/1002-0179.20140567

Video：

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Abstract Full text Figures/Tables Video References Cited by

Objective To investigate the expression of caspase-3 and Toll-like receptor 4 (TLR4) in the incised rat skin healing process and its relationship with the wound time and to provide an experimental evidence for the prediction of injury time. Methods After the rat incised wound model was established, hematoxylin-eosin dyeing technology and immunohistochemical staining technique were used to observe the expression of caspase-3 and TLR4. Then Image Pro Plus Image analysis software and SPSS statistical analysis software were used to deal with the experimental results. Results Caspase-3- and TLR4-positive cells were detected in epidermis, hair follicle and sebaceous gland cells in the control skin. The expression of caspase-3 and TLR4 of the ante mortem groups were significantly different compared with the control group except the 0 h group (P<0.05). Caspase-3- and TLR4-positive cells were detected in neutrophils around the hair follicle half an hour later. Caspase-3- and TLR4-positive cell rate increased with the infiltration of inflammatory cells. Caspase-3- and TLR4-positive cell rate reached the maximum on the 3 rd day, and then it began to decrease, and they were mainly expressed in fibroblasts and mononuclear macrophages. Caspase-3- and TLR4-positive cells were mainly expressed in fibroblasts on the 10th day. There was no significant differences between the postmortem injury groups and the normal control groups (P>0.05). Conclusion Caspase-3- and TLR4-positive cell rate is time dependent and stable in 25℃ temperature environment which makes it possible to determine the time of injury.

Citation： ZHANGDong-xue, GONGDao-yin, DAIHao, YUYou-jia, LUMei-gui, CAOYong, HUANGFei-jun. A Study on the Relationship between the Expression of Caspase-3 and Toll-like Receptor 4 and the Injury Time in Incised Rat Skin Healing. West China Medical Journal, 2014, 29(10): 1874-1878. doi: 10.7507/1002-0179.20140567 Copy

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12.	Tsung A, Hoffman RA, Izuishi K, et al. Hepatic ischemia/reperfusion injury involves functional TLR4 signaling in nonparenchymal cells[J]. J Immunol, 2007, 175(11):7661-7668.
13.	郝誠誠, 吳廣禮. 過度訓練可部分通過上調TLR4的表達激活死亡受體凋亡通路誘導大鼠腎小管上皮細胞凋亡[J]. 中國中西醫結合腎病雜志, 2012, 13(2):125-128.
14.	杜宇, 官大威, 趙銳. 皮膚切創愈合中caspase-3表達的免疫組化研究[J]. 法醫學雜志, 2004, 20(1):1-3.
15.	樓旭鵬, 馮瓊, 龔志強, 等. 皮膚切創愈合過程中TLR2、TLR4表達及其法醫學意義[J]. 法醫學雜志, 2007, 23(3):177-180, 184.

1. Kondo T, Ishida Y. Molecular pathology of wound healing[J]. Forensic Sci Int, 2010, 203(8):93-98.
2. Kluwe J, Mencin A, Schwabe RF. Toll-like receptors, wound healing, and carcinogenesis[J]. J Mol Med (Berl), 2009, 87(2):1-21.
3. Lu YC, Yeh WC, Ohashi PS. LPS/TLR4 signal transduction pathway[J]. Cytokine, 2008, 42(2):145-151.
4. 佟月, 高音, 張寶輝, 等. TLR4參與腦缺血再灌注小鼠海馬細胞凋亡[J]. 解剖科學進展, 2008, 14(4):372-376.
5. 戴昕, 李占全, 冀林華. 凋亡相關蛋白Caspase研究進展[J]. 中國現代醫藥雜志, 2010, 12(4):130-132.
6. 范鵬舉, 楊興華, 肖目張, 等. Toll樣受體4通過轉化生長因子β1參與增生性瘢痕形成的機制研究[J]. 生物化學與生物物理進展, 2011, 38(9):842-849.
7. Lye E, Mirtsos C, Suzuki N, et al. The role of interleukin 1 receptor-associated kinase-4(IRAK-4) kinase activity in IRAK-4-mediated signaling[J]. J Biol Chem, 2004, 279(39):40653-40658.
8. Miyake K. Innate immune sensing of pathogens and danger signals by cell surface Toll-like receptors[J]. Semin Immunol, 2007, 19(1):3-10.
9. 李俊, 曹樺, 李岡櫛, 等. Caspase 3活性改變對急性胰腺炎中性粒細胞凋亡的影響[J]. 華西醫學, 2007, 22(4):738-739.
10. Rassa JC, Meyers JL, Zhang Y, et al. Murine retroviruses activate B cells via interaction with toll-like receptor 4[J]. Proc Natl Acad Sci USA, 2002,99(4):2281-2286.
11. Lotze MT, Zeh HJ, Rubartelli A, et al. The grateful dead:damage-associated molecular pattern molecules and reduction/oxidation regulate immunity[J]. Immunol Rev, 2007, 220(1):60-81.
12. Tsung A, Hoffman RA, Izuishi K, et al. Hepatic ischemia/reperfusion injury involves functional TLR4 signaling in nonparenchymal cells[J]. J Immunol, 2007, 175(11):7661-7668.
13. 郝誠誠, 吳廣禮. 過度訓練可部分通過上調TLR4的表達激活死亡受體凋亡通路誘導大鼠腎小管上皮細胞凋亡[J]. 中國中西醫結合腎病雜志, 2012, 13(2):125-128.
14. 杜宇, 官大威, 趙銳. 皮膚切創愈合中caspase-3表達的免疫組化研究[J]. 法醫學雜志, 2004, 20(1):1-3.
15. 樓旭鵬, 馮瓊, 龔志強, 等. 皮膚切創愈合過程中TLR2、TLR4表達及其法醫學意義[J]. 法醫學雜志, 2007, 23(3):177-180, 184.

West China Medical Journal

A Study on the Relationship between the Expression of Caspase-3 and Toll-like Receptor 4 and the Injury Time in Incised Rat Skin Healing

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