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

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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.	郝诚诚, 吴广礼. 过度训练可部分通过上调TLR4的表达激活死亡受体凋亡通路诱导大鼠肾小管上皮细胞凋亡[J]. 中国中西医结合肾病杂志, 2012, 13(2):125-128.
14.	杜宇, 官大威, 赵锐. 皮肤切创愈合中caspase-3表达的免疫组化研究[J]. 法医学杂志, 2004, 20(1):1-3.
15.	楼旭鹏, 冯琼, 龚志强, 等. 皮肤切创愈合过程中TLR2、TLR4表达及其法医学意义[J]. 法医学杂志, 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, 张宝辉, 等. TLR4参与脑缺血再灌注小鼠海马细胞凋亡[J]. 解剖科学进展, 2008, 14(4):372-376.
5. 戴昕, 李占全, 冀林华. 凋亡相关蛋白Caspase研究进展[J]. 中国现代医药杂志, 2010, 12(4):130-132.
6. 范鹏举, 杨兴华, 肖目张, 等. Toll样受体4通过转化生长因子β1参与增生性瘢痕形成的机制研究[J]. 生物化学与生物物理进展, 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, 曹桦, 李冈栉, 等. Caspase 3活性改变对急性胰腺炎中性粒细胞凋亡的影响[J]. 华西医学, 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. 郝诚诚, 吴广礼. 过度训练可部分通过上调TLR4的表达激活死亡受体凋亡通路诱导大鼠肾小管上皮细胞凋亡[J]. 中国中西医结合肾病杂志, 2012, 13(2):125-128.
14. 杜宇, 官大威, 赵锐. 皮肤切创愈合中caspase-3表达的免疫组化研究[J]. 法医学杂志, 2004, 20(1):1-3.
15. 楼旭鹏, 冯琼, 龚志强, 等. 皮肤切创愈合过程中TLR2、TLR4表达及其法医学意义[J]. 法医学杂志, 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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