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Wogonin Attenuates Liver Fibrosis Via Regulating Hepatic Stellate Cell

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Wogonin Attenuates Liver Fibrosis Via Regulating Hepatic Stellate Cell International Immunopharmacology 75 (2019) 105671 Contents lists available at ScienceDirect International Immunopharmacology journal homepage: www.elsevier.com/locate/intimp Wogonin attenuates liver fibrosis via regulating hepatic stellate cell T activation and apoptosis Xiao-Sa Du, Hai-Di Li, Xiao-Juan Yang, Juan-Juan Li, Jie-Jie Xu, Yu Chen, Qing-Qing Xu, ⁎ Lei Yang, Chang-Sheng He, Cheng Huang, Xiao-Ming Meng, Jun Li The Key Laboratory of Major Autoimmune Diseases, Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, China The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Institute for Liver Diseases of Anhui Medical University, China School of Pharmacy, Anhui Key Laboratory of Bioactivity of Natural Products, Anhui Medical University, Hefei 230032, China ARTICLE INFO ABSTRACT Keywords: Liver fibrosis is the representative features of liver chronic inflammation and the characteristic of early cirrhosis. Wogonin To date, effective therapy for liver fibrosis is lacking. Recently, Traditional Chinese Medicine (TCM)hasat- Liver fibrosis tracted increasing attention due to its wide pharmacological effects and more uses in clinical. Wogonin, asone Hepatic stellate cells (HSCs) major active constituent of Scutellaria radix, has been reported it plays an important role in anti-inflammatory, Apoptosis anti-cancer, anti-viral, anti-angiogenesis, anti-oxidant and neuro-protective effects. However, the anti-fibrotic effect of wogonin is never covered in liver. In this study, we evaluated the protect effect of wogonininliver fibrosis. Wogonin significantly attenuated liver fibrosis both4 inCCl -induced mice and TGF-β1 activated HSCs. Meanwhile, wogonin can enhances apoptosis of TGF-β1 activated HSC-T6 cell from rat and LX-2 cell from human detected by flow cytometry. Additionally, wogonin can largely enhances cle-caspase3, cle-caspase9 expression and the ratio of Bax/Bcl-2 in T6 cells. Pro-apoptosis effect of wogonin in vivo was further verified in situ. In conclusion, wogonin can attenuate liver fibrosis via regulating the activation and apoptosis of hepatic stellate cells, and may be an effective drug to treat and prevent liver fibrosis. 1. Introduction death process [14], accompanied by DNA division, cell atrophy, and other phenotypes [15]. There are many enzymatic bases of apoptosis, Liver fibrosis is an adaptive response to liver injuries to maintaining among which caspase family [16–18] and Bcl-2 [16,19] family are liver integrity [1]. Clinically, the progression of liver fibrosis including closely related to apoptosis. cirrhosis and liver cancer has become a serious social problem [2]. With the increasing emphasis, many TCMs have been reported to Many causes including viral infection, non-alcoholic fatty liver disease, promote cell apoptosis, among of them wogonin has also been reported alcoholic liver disease, drug toxicity, metabolic disorders, autoimmune to promote apoptosis in liver cancer cells [20]. Wogonin (5,7-dihy- disease can result in liver fibrosis [3,4]. In the recent years, liver fibrosis droxy-8-methoxyflavone), one of the main active ingredients ofScu- attracted increasing attention because it is a major cause of liver cir- tellaria radix, is a kind of flavonoid compound [21,22]. It has been rhosis, with organ failure and high mortality [5,6]. It is characterized involved in the occurrence and treatment of many diseases and has with activation of hepatic stellate cells (HSCs) and excessive deposition wide ranges of pharmacological activities including anti-inflammation of extracellular matrix (ECM) [7,8]. Quiescent HSCs in the perisinu- [23–25], anti-angiogenesis [26], anti-virus [21,27], anti-fibrosis soidal space of Disse filled with thin permeable connective tissue are [28,29], anti-cancer [30] and leukemia [31,32]. Studies have showed activated and differentiated into myofibroblasts characterized byup- that wogonin plays a role in promoting apoptosis of liver cancer cells regulation of α-SMA and Coll-α1 during liver fibrosis [9,10]. Therefore, through Bax/Bcl-2 [20]. In addition, wogonin can inhibit the fibrosis of the activation and proliferation of HSCs play crucial roles in the de- renal tubular epithelial cells [28], but wogonin has never been studied velopment of liver fibrosis [11]. Evidences reveal that inhibiting pro- in liver fibrosis. Thus, we studied the protective role of wogonin in liver liferation, activation of HSCs and promoting HSCs apoptosis may be- fibrosis by regulating the apoptosis of hepatic stellate cells. come a key therapy strategy for liver fibrosis [12,13]. Apoptosis, a unique style of cell death, regulate programmed cell ⁎ Corresponding author at: School of Pharmacy, Anhui Medical University. Hefei, Anhui, China. E-mail address: [email protected] (J. Li). https://doi.org/10.1016/j.intimp.2019.05.056 Received 28 January 2019; Received in revised form 28 May 2019; Accepted 28 May 2019 Available online 01 August 2019 1567-5769/ © 2019 Elsevier B.V. All rights reserved. X.-S. Du, et al. International Immunopharmacology 75 (2019) 105671 Table 1 Primers sequences used for real-time q-PCR. Gene Forward Reverse Mouse α-SMA 5′-CGGGAGAAAATGACCCAGATT-3′ 5′-AGGGACAGCACAGCCTGAATAG-3′ Human α-SMA 5′-CAGGAAGGACCTGTATGCCA-3′ 5′-TGATCTTCATGGTGCTGGGT-3′ Rat α-SMA 5′-CAATGGCTCCGGGCTCTGTA-3′ 5′-CTCTTGCTCTGCGCTTCGTC-3′ Mouse Coll-α1 5′-GGAGAGTACTGGATCGACCCTAAC-3′ 5′-ACACAGGTCTGACCTGTCTCCAT-3′ Human Coll-α1 5′-CACCAATCACCTGCGTACAG-3′ 5′-GCAGTTCTTGGTCTCGTCAC-3′ Rat Coll-α1 5′-ACCTCAGGGTATTGCTGGAC-3′ 5′-GACCAGGGAAGCCTCTTTCT-3′ Mouse β-actin 5′-CATTGCTGACAGGATGCAGAA-3′ 5′-ATGGTGCTAGGAGCCAGAGC-3′ Human β-actin 5′-GGGAAATCGTGCGTGACATTAAGG-3′ 5-CAGGAAGGAAGGCTGGAAGAGTG-3′ Rat β-actin 5′-CCCATCTATGAGGGTTACGC-3′ 5′-TTTAATGTCACGCACGATTTC-3′ 2. Materials and methods 2.2. Animal treatment 2.1. Reagents and antibodies Six-week-old male C57BL/6 mice (n = 72) weighting 18–22 g, were provided from the Experimental Animal Center of Anhui Medical 2.1.1. Reagents University. The animal experimental protocol was reviewed and ap- proved by the University Animal Care and Use Committee. And all mice Reagents Supplier Cat. no. were housed in comfortable environment and were acclimatized for Wogonin (purity > 98%) Meilune Biology Technology MB6663, 3 days before the experiment. Total mice were randomly divided into 6 (DaLian, China) CAS 632-85-9 groups (n = 12 per group) including control group, CCl4 group, CCl4 ≧ Colchicine (purity 98%) Target Molecule (Boston, USA) T0320, group treated with wogonin (10 mg/kg, 20 mg/kg, 40 mg/kg), CCl4 CAS 64-86-8 group treated with colchicine (0.32 mg/kg). CCl4 group and treatment TGF-β1 Pepro Tech Inc. (Rocky Hill, USA) 500-M66 Dimethyl sulfoxide Sigma Chemical (Sigma-Aldrich, 67-68-5 group were subjected intraperitoneal injections of olive oil with 20% USA) CCl4 (2.5 ml/kg weight) for 2 times per week up to 4 weeks to induce Methyl thiazolyl tetrazolium Sigma Chemical (Sigma-Aldrich, 57,360–69-7 liver fibrosis model, and before intraperitoneal injection4 ofCCl , mice USA) in treatment group were injected intraperitoneally different con- ALT assay kit Jiancheng Biology Institution C009-2 centrations of wogonin and colchicine for 5 days, control group were PeproTech (Nanjing, Jiangsu, China) injected intraperitoneally the same olive oil. AST assay kit Jiancheng Biology Institution C010-2 PeproTech (Nanjing, Jiangsu, China) 2.3. ALT/AST activity assay Annexin V-FITC Cell apop- BestBio (Shanghai, China) BB-4101-3 tosis kit Cell cycle and apoptosis an- Beyotime (China) C1052 The levels of ALT and AST in serum from each group mice were alysis kit assayed by using the corresponding activity assay kits according to the In Situ Cell Death Detection Roche (Switzerland) 11684817910 manufacturer's instruction. The absorbance was detected with a Kit Multiskan MK3 (Biotek, USA) at 510 nm. Pronase E Sigma Chemical (Sigma-Aldrich, P6911 USA) Collagenase IV Sigma Chemical (Sigma-Aldrich, C5138 USA) 2.4. Histopathology and immunohistochemistry staining Hepes Caisson Labs (USA) H006-100GM Nycodenz Axis-shield (Norway) AS1002424 The suitable size of each group was soaked in 4% polyformaldehyde for 24 h, then were paraffin embedding. Permanent tissue was cut (5μm 2.1.2. Antibodies thick) to stain with hematoxylin and eosin (H&E), masson, and im- munohistochemical (IHC) staining of α-SMA. Uniform distribution of Antibody Supplier Cat. no. hepatocytes, size of intercellular spaces and infiltration of inflammatory α-SMA CST (USA) 19245S cells in portal area were evaluated by HE staining. The formation of Coll-α1 Bioss (China) bs-7158R fibrosis connective tissue and destruction of hepatic lobule structure Caspase3 CST (USA) 9662S were observed by Masson staining. Fibrosis indicator α-SMA was de- Caspase9 CST (USA) 9504S tected by IHC. Finally, the dyeing section were observed and photo- Bax Abcam (USA) ab32503 Bcl-2 Abcam (USA) ab59348 graphed by light microscopy. β-Actin ZSGB-BIO (Beijing, China) TA-09 2 X.-S. Du, et al. International Immunopharmacology 75 (2019) 105671 (caption on next page) 3 X.-S. Du, et al. International Immunopharmacology 75 (2019) 105671 Fig. 1. Wogonin attenuates liver injury induced by CCl4 in mice. A: Liver appearance of mice in each group, including control group, CCl4-treated mice, 10 mg/kg, 20 mg/kg, 40 mg/kg wogonin-treated mice and positive-treated mice (colchicine, 0.32 mg/kg). B and C: Hematoxylin and eosin (H&E) staining and Masson staining of liver tissues in different groups. D: Immunohistochemistry of α-SMA in different groups of liver tissues. E and F: Serum ALT and AST levels ofmiceineachgroup. The values were represented by means ± SD at least 6 separate experimental. *P < 0.05, **P < 0.01, ***P < 0.001 compared to control mice. #P < 0.05, ## ### P < 0.01, P < 0.001 compared to CCl4-treated mice. Wog: wogonin, Col: Colchicine. 2.5. TUNEL staining 2.7. Cell culture and cell treatment The paraffin-embedded liver tissue of each group were dewaxed and T6-hepatic stellate cells of rats, LX2-liver stellate cells of humans washed slices before repaired with protease K at 37 °C for 25 min.
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