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Effect of interferon-γ and tumor necrosis factor-α on hepatitis B virus following lamivudine treatment
AIM: To evaluate anti-hepatitis B virus (HBV) activity and cytotoxicity of interferon-α, (IFN-3,) and tumor ne- crosis factor-α (TNF-α) following lamivudine treatment of HepG2.2.15 cells. METHODS: HepG2.2.15 cells were treated with 2 pmol/L lamivudine for 16 d (lamivudine group), cultured for 10 d,...
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Published in: | World journal of gastroenterology : WJG 2012-07, Vol.18 (27), p.3617-3622 |
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description | AIM: To evaluate anti-hepatitis B virus (HBV) activity and cytotoxicity of interferon-α, (IFN-3,) and tumor ne- crosis factor-α (TNF-α) following lamivudine treatment of HepG2.2.15 cells. METHODS: HepG2.2.15 cells were treated with 2 pmol/L lamivudine for 16 d (lamivudine group), cultured for 10 d, followed by 5 ng/ml TNF-α and 1000 U/mL IFN-γ, for 6 d (cytokine group), or treated with 2 ~tmol/L lami- vudine for 10 d followed by 5 ng/mL TNF-α and 1000 U/mL IFN-γ, for 6 d (sequential group), or cultured without additions for 16 d (control group). Intracellular DNA was extracted from 3 ×10^ HepG2.2.15 cells from each group. The extracted DNA was further purified with mung bean nuclease to remove HBV relaxed circu- lar DNA that may have remained. Both HBV covalently closed circular DNA (cccDNA) and HBV DNA were exam- ined with real-time polymerase chain reaction. The titers of hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) were quantified with enzyme-linkedimmunosorbent assay. Cell viability was measured with the cell counting kit-8 assay. RESULTS: Compared to lamivudine alone (22.63%±0.12%), both sequential (51.50% ± 0.17%, P = 0.034) and cytokine treatment (49.66% ± 0.06%, P = 0.041) showed a stronger inhibition of HBV cccDNA; the dif- ference between the.sequential and cytokine groups was not statistically significant (51.50% ± 0.17% vs 49.66% ± 0.06%, P = 0.88). The sequential group showed less inhibition of HBV DNA replication than the lamivudine group (67.47% ±0.02% vs 82.48% ± 0.05%, P = 0.014); the difference between the sequen- tial and cytokine groups was not statistically significant (67.47% ± 0.02% vs 57.45% ± 0.07%, P = 0.071). The levels of HBsAg and HBeAg were significantly de- creased in the sequential treatment group compared to the other groups [HBsAg: 3.48 ± 0.04 (control), 3.09 ± 0.08 (lamivudine), 2.55± 0.13 (cytokine), 2.32 ± 0.08 (sequential), P = 0.042 for each between-group comparison; HBeAg 3.48 ± 0.01 (control), 3.08 ± 0.08 (lamivudine), 2.57 ± 0.15 (cytokine), 2.34 ± 0.12 (se- quential), P = 0.048 for each between-group compari- son]. Cell viability in the cytokine group was reduced to 58.03% ± 8.03% compared with control cells (58.03% ± 8.03% vs 100%, P = 0.000). Lamivudine pretreat- ment significantly reduced IFN-γ, ± TNF-αmediated toxicity of HepG2.2.15 cells [85.82% =1= 5.43% (sequen- tial) vs 58.03% ± 8.03% (cytokine), P = 0.002]. CONCLUSION: Sequential treatment overcame the lower ability of lamivudine |
doi_str_mv | 10.3748/wjg.v18.i27.3617 |
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fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3400866</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>42811731</cqvip_id><sourcerecordid>22826629</sourcerecordid><originalsourceid>FETCH-LOGICAL-c422t-35badc3e7f649faa18ba4feb9e77963b10e9044491c6ead7ec975931d7697efb3</originalsourceid><addsrcrecordid>eNpVkM9OGzEQhy1URNKUO6fKfYAN_hd7fanURoEiIXGhZ8u7O06Mdu3U6wTxWFXfg2fCETSC00gz8_tG8yF0QcmcK1FfPj6s53tazz1Tcy6pOkFTxqiuWC3IJzSlhKhKc6Ym6PM4PhDCOF-wMzRhrGZSMj1Fm5Vz0GYcHfYhQ3KQYqie_2EbOpx3Q0w4QJvi6EfsbJtjqp7_4hjwBrY2-1zaP_Hep10Zx76Pjz6scW8Hv991PgDOCWweIOQv6NTZfoTztzpDv69W98tf1e3d9c3yx23VCsZyxReN7VoOykmhnbW0bqxw0GhQSkveUAKaCCE0bSXYTkGr1UJz2impFbiGz9D3V-521wzQteV0sr3ZJj_Y9GSi9ebjJPiNWce94YKQWsoCIK-Aw9djAnfMUmIO1k2xbop1U6ybg_US-fr-5jHwX3NZ-PbG3MSw_lMcHXcEq2lBUP4CvXqPyg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Effect of interferon-γ and tumor necrosis factor-α on hepatitis B virus following lamivudine treatment</title><source>Open Access: PubMed Central</source><creator>Shi, Hong ; Lu, Lu ; Zhang, Ning-Ping ; Zhang, Shun-Cai ; Shen, Xi-Zhong</creator><creatorcontrib>Shi, Hong ; Lu, Lu ; Zhang, Ning-Ping ; Zhang, Shun-Cai ; Shen, Xi-Zhong</creatorcontrib><description>AIM: To evaluate anti-hepatitis B virus (HBV) activity and cytotoxicity of interferon-α, (IFN-3,) and tumor ne- crosis factor-α (TNF-α) following lamivudine treatment of HepG2.2.15 cells. METHODS: HepG2.2.15 cells were treated with 2 pmol/L lamivudine for 16 d (lamivudine group), cultured for 10 d, followed by 5 ng/ml TNF-α and 1000 U/mL IFN-γ, for 6 d (cytokine group), or treated with 2 ~tmol/L lami- vudine for 10 d followed by 5 ng/mL TNF-α and 1000 U/mL IFN-γ, for 6 d (sequential group), or cultured without additions for 16 d (control group). Intracellular DNA was extracted from 3 ×10^ HepG2.2.15 cells from each group. The extracted DNA was further purified with mung bean nuclease to remove HBV relaxed circu- lar DNA that may have remained. Both HBV covalently closed circular DNA (cccDNA) and HBV DNA were exam- ined with real-time polymerase chain reaction. The titers of hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) were quantified with enzyme-linkedimmunosorbent assay. Cell viability was measured with the cell counting kit-8 assay. RESULTS: Compared to lamivudine alone (22.63%±0.12%), both sequential (51.50% ± 0.17%, P = 0.034) and cytokine treatment (49.66% ± 0.06%, P = 0.041) showed a stronger inhibition of HBV cccDNA; the dif- ference between the.sequential and cytokine groups was not statistically significant (51.50% ± 0.17% vs 49.66% ± 0.06%, P = 0.88). The sequential group showed less inhibition of HBV DNA replication than the lamivudine group (67.47% ±0.02% vs 82.48% ± 0.05%, P = 0.014); the difference between the sequen- tial and cytokine groups was not statistically significant (67.47% ± 0.02% vs 57.45% ± 0.07%, P = 0.071). The levels of HBsAg and HBeAg were significantly de- creased in the sequential treatment group compared to the other groups [HBsAg: 3.48 ± 0.04 (control), 3.09 ± 0.08 (lamivudine), 2.55± 0.13 (cytokine), 2.32 ± 0.08 (sequential), P = 0.042 for each between-group comparison; HBeAg 3.48 ± 0.01 (control), 3.08 ± 0.08 (lamivudine), 2.57 ± 0.15 (cytokine), 2.34 ± 0.12 (se- quential), P = 0.048 for each between-group compari- son]. Cell viability in the cytokine group was reduced to 58.03% ± 8.03% compared with control cells (58.03% ± 8.03% vs 100%, P = 0.000). Lamivudine pretreat- ment significantly reduced IFN-γ, ± TNF-αmediated toxicity of HepG2.2.15 cells [85.82% =1= 5.43% (sequen- tial) vs 58.03% ± 8.03% (cytokine), P = 0.002]. CONCLUSION: Sequential treatment overcame the lower ability of lamivudine alone to inhibit cccDNA and precluded the aggressive cytotoxicity involving IFN-y and TNF-α by decreasing the viral load.</description><identifier>ISSN: 1007-9327</identifier><identifier>EISSN: 2219-2840</identifier><identifier>DOI: 10.3748/wjg.v18.i27.3617</identifier><identifier>PMID: 22826629</identifier><language>eng</language><publisher>United States: Baishideng Publishing Group Co., Limited</publisher><subject>Antiviral Agents - pharmacology ; Brief ; Cell Survival - drug effects ; DNA Replication - drug effects ; DNA, Viral - biosynthesis ; DNA, Viral - drug effects ; Enzyme-Linked Immunosorbent Assay ; Hep G2 Cells ; Hepatitis B e Antigens - metabolism ; Hepatitis B Surface Antigens - metabolism ; Hepatitis B virus - drug effects ; Hepatitis B virus - genetics ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; Hepatocytes - pathology ; Hepatocytes - virology ; HepG2细胞 ; Humans ; Interferon-gamma - pharmacology ; Lamivudine - pharmacology ; Real-Time Polymerase Chain Reaction ; Recombinant Proteins - pharmacology ; Time Factors ; Transfection ; Tumor Necrosis Factor-alpha - pharmacology ; Viral Load ; Virus Replication - drug effects ; 乙型肝炎表面抗原 ; 干扰素 ; 拉米夫定 ; 治疗 ; 肝炎病毒 ; 肿瘤坏死因子</subject><ispartof>World journal of gastroenterology : WJG, 2012-07, Vol.18 (27), p.3617-3622</ispartof><rights>2012 Baishideng Publishing Group Co., Limited. All rights reserved. 2012</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-35badc3e7f649faa18ba4feb9e77963b10e9044491c6ead7ec975931d7697efb3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/84123X/84123X.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3400866/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3400866/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22826629$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Hong</creatorcontrib><creatorcontrib>Lu, Lu</creatorcontrib><creatorcontrib>Zhang, Ning-Ping</creatorcontrib><creatorcontrib>Zhang, Shun-Cai</creatorcontrib><creatorcontrib>Shen, Xi-Zhong</creatorcontrib><title>Effect of interferon-γ and tumor necrosis factor-α on hepatitis B virus following lamivudine treatment</title><title>World journal of gastroenterology : WJG</title><addtitle>World Journal of Gastroenterology</addtitle><description>AIM: To evaluate anti-hepatitis B virus (HBV) activity and cytotoxicity of interferon-α, (IFN-3,) and tumor ne- crosis factor-α (TNF-α) following lamivudine treatment of HepG2.2.15 cells. METHODS: HepG2.2.15 cells were treated with 2 pmol/L lamivudine for 16 d (lamivudine group), cultured for 10 d, followed by 5 ng/ml TNF-α and 1000 U/mL IFN-γ, for 6 d (cytokine group), or treated with 2 ~tmol/L lami- vudine for 10 d followed by 5 ng/mL TNF-α and 1000 U/mL IFN-γ, for 6 d (sequential group), or cultured without additions for 16 d (control group). Intracellular DNA was extracted from 3 ×10^ HepG2.2.15 cells from each group. The extracted DNA was further purified with mung bean nuclease to remove HBV relaxed circu- lar DNA that may have remained. Both HBV covalently closed circular DNA (cccDNA) and HBV DNA were exam- ined with real-time polymerase chain reaction. The titers of hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) were quantified with enzyme-linkedimmunosorbent assay. Cell viability was measured with the cell counting kit-8 assay. RESULTS: Compared to lamivudine alone (22.63%±0.12%), both sequential (51.50% ± 0.17%, P = 0.034) and cytokine treatment (49.66% ± 0.06%, P = 0.041) showed a stronger inhibition of HBV cccDNA; the dif- ference between the.sequential and cytokine groups was not statistically significant (51.50% ± 0.17% vs 49.66% ± 0.06%, P = 0.88). The sequential group showed less inhibition of HBV DNA replication than the lamivudine group (67.47% ±0.02% vs 82.48% ± 0.05%, P = 0.014); the difference between the sequen- tial and cytokine groups was not statistically significant (67.47% ± 0.02% vs 57.45% ± 0.07%, P = 0.071). The levels of HBsAg and HBeAg were significantly de- creased in the sequential treatment group compared to the other groups [HBsAg: 3.48 ± 0.04 (control), 3.09 ± 0.08 (lamivudine), 2.55± 0.13 (cytokine), 2.32 ± 0.08 (sequential), P = 0.042 for each between-group comparison; HBeAg 3.48 ± 0.01 (control), 3.08 ± 0.08 (lamivudine), 2.57 ± 0.15 (cytokine), 2.34 ± 0.12 (se- quential), P = 0.048 for each between-group compari- son]. Cell viability in the cytokine group was reduced to 58.03% ± 8.03% compared with control cells (58.03% ± 8.03% vs 100%, P = 0.000). Lamivudine pretreat- ment significantly reduced IFN-γ, ± TNF-αmediated toxicity of HepG2.2.15 cells [85.82% =1= 5.43% (sequen- tial) vs 58.03% ± 8.03% (cytokine), P = 0.002]. CONCLUSION: Sequential treatment overcame the lower ability of lamivudine alone to inhibit cccDNA and precluded the aggressive cytotoxicity involving IFN-y and TNF-α by decreasing the viral load.</description><subject>Antiviral Agents - pharmacology</subject><subject>Brief</subject><subject>Cell Survival - drug effects</subject><subject>DNA Replication - drug effects</subject><subject>DNA, Viral - biosynthesis</subject><subject>DNA, Viral - drug effects</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Hep G2 Cells</subject><subject>Hepatitis B e Antigens - metabolism</subject><subject>Hepatitis B Surface Antigens - metabolism</subject><subject>Hepatitis B virus - drug effects</subject><subject>Hepatitis B virus - genetics</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>Hepatocytes - pathology</subject><subject>Hepatocytes - virology</subject><subject>HepG2细胞</subject><subject>Humans</subject><subject>Interferon-gamma - pharmacology</subject><subject>Lamivudine - pharmacology</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Time Factors</subject><subject>Transfection</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Viral Load</subject><subject>Virus Replication - drug effects</subject><subject>乙型肝炎表面抗原</subject><subject>干扰素</subject><subject>拉米夫定</subject><subject>治疗</subject><subject>肝炎病毒</subject><subject>肿瘤坏死因子</subject><issn>1007-9327</issn><issn>2219-2840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNpVkM9OGzEQhy1URNKUO6fKfYAN_hd7fanURoEiIXGhZ8u7O06Mdu3U6wTxWFXfg2fCETSC00gz8_tG8yF0QcmcK1FfPj6s53tazz1Tcy6pOkFTxqiuWC3IJzSlhKhKc6Ym6PM4PhDCOF-wMzRhrGZSMj1Fm5Vz0GYcHfYhQ3KQYqie_2EbOpx3Q0w4QJvi6EfsbJtjqp7_4hjwBrY2-1zaP_Hep10Zx76Pjz6scW8Hv991PgDOCWweIOQv6NTZfoTztzpDv69W98tf1e3d9c3yx23VCsZyxReN7VoOykmhnbW0bqxw0GhQSkveUAKaCCE0bSXYTkGr1UJz2impFbiGz9D3V-521wzQteV0sr3ZJj_Y9GSi9ebjJPiNWce94YKQWsoCIK-Aw9djAnfMUmIO1k2xbop1U6ybg_US-fr-5jHwX3NZ-PbG3MSw_lMcHXcEq2lBUP4CvXqPyg</recordid><startdate>20120721</startdate><enddate>20120721</enddate><creator>Shi, Hong</creator><creator>Lu, Lu</creator><creator>Zhang, Ning-Ping</creator><creator>Zhang, Shun-Cai</creator><creator>Shen, Xi-Zhong</creator><general>Baishideng Publishing Group Co., Limited</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20120721</creationdate><title>Effect of interferon-γ and tumor necrosis factor-α on hepatitis B virus following lamivudine treatment</title><author>Shi, Hong ; Lu, Lu ; Zhang, Ning-Ping ; Zhang, Shun-Cai ; Shen, Xi-Zhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-35badc3e7f649faa18ba4feb9e77963b10e9044491c6ead7ec975931d7697efb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Antiviral Agents - pharmacology</topic><topic>Brief</topic><topic>Cell Survival - drug effects</topic><topic>DNA Replication - drug effects</topic><topic>DNA, Viral - biosynthesis</topic><topic>DNA, Viral - drug effects</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Hep G2 Cells</topic><topic>Hepatitis B e Antigens - metabolism</topic><topic>Hepatitis B Surface Antigens - metabolism</topic><topic>Hepatitis B virus - drug effects</topic><topic>Hepatitis B virus - genetics</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>Hepatocytes - pathology</topic><topic>Hepatocytes - virology</topic><topic>HepG2细胞</topic><topic>Humans</topic><topic>Interferon-gamma - pharmacology</topic><topic>Lamivudine - pharmacology</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Time Factors</topic><topic>Transfection</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Viral Load</topic><topic>Virus Replication - drug effects</topic><topic>乙型肝炎表面抗原</topic><topic>干扰素</topic><topic>拉米夫定</topic><topic>治疗</topic><topic>肝炎病毒</topic><topic>肿瘤坏死因子</topic><toplevel>online_resources</toplevel><creatorcontrib>Shi, Hong</creatorcontrib><creatorcontrib>Lu, Lu</creatorcontrib><creatorcontrib>Zhang, Ning-Ping</creatorcontrib><creatorcontrib>Zhang, Shun-Cai</creatorcontrib><creatorcontrib>Shen, Xi-Zhong</creatorcontrib><collection>维普_期刊</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>World journal of gastroenterology : WJG</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, Hong</au><au>Lu, Lu</au><au>Zhang, Ning-Ping</au><au>Zhang, Shun-Cai</au><au>Shen, Xi-Zhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of interferon-γ and tumor necrosis factor-α on hepatitis B virus following lamivudine treatment</atitle><jtitle>World journal of gastroenterology : WJG</jtitle><addtitle>World Journal of Gastroenterology</addtitle><date>2012-07-21</date><risdate>2012</risdate><volume>18</volume><issue>27</issue><spage>3617</spage><epage>3622</epage><pages>3617-3622</pages><issn>1007-9327</issn><eissn>2219-2840</eissn><abstract>AIM: To evaluate anti-hepatitis B virus (HBV) activity and cytotoxicity of interferon-α, (IFN-3,) and tumor ne- crosis factor-α (TNF-α) following lamivudine treatment of HepG2.2.15 cells. METHODS: HepG2.2.15 cells were treated with 2 pmol/L lamivudine for 16 d (lamivudine group), cultured for 10 d, followed by 5 ng/ml TNF-α and 1000 U/mL IFN-γ, for 6 d (cytokine group), or treated with 2 ~tmol/L lami- vudine for 10 d followed by 5 ng/mL TNF-α and 1000 U/mL IFN-γ, for 6 d (sequential group), or cultured without additions for 16 d (control group). Intracellular DNA was extracted from 3 ×10^ HepG2.2.15 cells from each group. The extracted DNA was further purified with mung bean nuclease to remove HBV relaxed circu- lar DNA that may have remained. Both HBV covalently closed circular DNA (cccDNA) and HBV DNA were exam- ined with real-time polymerase chain reaction. The titers of hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) were quantified with enzyme-linkedimmunosorbent assay. Cell viability was measured with the cell counting kit-8 assay. RESULTS: Compared to lamivudine alone (22.63%±0.12%), both sequential (51.50% ± 0.17%, P = 0.034) and cytokine treatment (49.66% ± 0.06%, P = 0.041) showed a stronger inhibition of HBV cccDNA; the dif- ference between the.sequential and cytokine groups was not statistically significant (51.50% ± 0.17% vs 49.66% ± 0.06%, P = 0.88). The sequential group showed less inhibition of HBV DNA replication than the lamivudine group (67.47% ±0.02% vs 82.48% ± 0.05%, P = 0.014); the difference between the sequen- tial and cytokine groups was not statistically significant (67.47% ± 0.02% vs 57.45% ± 0.07%, P = 0.071). The levels of HBsAg and HBeAg were significantly de- creased in the sequential treatment group compared to the other groups [HBsAg: 3.48 ± 0.04 (control), 3.09 ± 0.08 (lamivudine), 2.55± 0.13 (cytokine), 2.32 ± 0.08 (sequential), P = 0.042 for each between-group comparison; HBeAg 3.48 ± 0.01 (control), 3.08 ± 0.08 (lamivudine), 2.57 ± 0.15 (cytokine), 2.34 ± 0.12 (se- quential), P = 0.048 for each between-group compari- son]. Cell viability in the cytokine group was reduced to 58.03% ± 8.03% compared with control cells (58.03% ± 8.03% vs 100%, P = 0.000). Lamivudine pretreat- ment significantly reduced IFN-γ, ± TNF-αmediated toxicity of HepG2.2.15 cells [85.82% =1= 5.43% (sequen- tial) vs 58.03% ± 8.03% (cytokine), P = 0.002]. CONCLUSION: Sequential treatment overcame the lower ability of lamivudine alone to inhibit cccDNA and precluded the aggressive cytotoxicity involving IFN-y and TNF-α by decreasing the viral load.</abstract><cop>United States</cop><pub>Baishideng Publishing Group Co., Limited</pub><pmid>22826629</pmid><doi>10.3748/wjg.v18.i27.3617</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Antiviral Agents - pharmacology Brief Cell Survival - drug effects DNA Replication - drug effects DNA, Viral - biosynthesis DNA, Viral - drug effects Enzyme-Linked Immunosorbent Assay Hep G2 Cells Hepatitis B e Antigens - metabolism Hepatitis B Surface Antigens - metabolism Hepatitis B virus - drug effects Hepatitis B virus - genetics Hepatocytes - drug effects Hepatocytes - metabolism Hepatocytes - pathology Hepatocytes - virology HepG2细胞 Humans Interferon-gamma - pharmacology Lamivudine - pharmacology Real-Time Polymerase Chain Reaction Recombinant Proteins - pharmacology Time Factors Transfection Tumor Necrosis Factor-alpha - pharmacology Viral Load Virus Replication - drug effects 乙型肝炎表面抗原 干扰素 拉米夫定 治疗 肝炎病毒 肿瘤坏死因子 |
title | Effect of interferon-γ and tumor necrosis factor-α on hepatitis B virus following lamivudine treatment |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T21%3A24%3A48IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Effect%20of%20interferon-%CE%B3%20and%20tumor%20necrosis%20factor-%CE%B1%20on%20hepatitis%20B%20virus%20following%20lamivudine%20treatment&rft.jtitle=World%20journal%20of%20gastroenterology%20:%20WJG&rft.au=Shi,%20Hong&rft.date=2012-07-21&rft.volume=18&rft.issue=27&rft.spage=3617&rft.epage=3622&rft.pages=3617-3622&rft.issn=1007-9327&rft.eissn=2219-2840&rft_id=info:doi/10.3748/wjg.v18.i27.3617&rft_dat=%3Cpubmed_cross%3E22826629%3C/pubmed_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c422t-35badc3e7f649faa18ba4feb9e77963b10e9044491c6ead7ec975931d7697efb3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_id=info:pmid/22826629&rft_cqvip_id=42811731&rfr_iscdi=true |