Bangladesh Journal of Pharmacology
https://www.banglajol.info:443/index.php/BJP
<p>Bangladesh Journal of Pharmacology (Bangladesh J Pharmacol) is an open access, video component, single blinded peer-reviewed journal of the Bangladesh Pharmacological Society (BDPS). We publish Research article, Mini-review, Meta-analysis, Clinical Trial, Visual Experiment and Letter to the Editor. <br> The author will not be charged in the form of submission fee, article processing fee or publication fee. It is completely free. We do not publish any advertisement.</p> <p><strong>Journal Metrics</strong><br> Journal metrics allow you to compare journals, regardless of their subject classification.<br>Impact Factor<sup>®</sup> as reported in the 2019 Journal Citation Reports<sup>®</sup> (Clarivate Analytics, 2020): <strong>1.306</strong></p> <p><img src="/public/site/images/misbah/IF1.png"></p> <p>CiteScore (2019): <strong>2.0</strong> <a href="https://www.scopus.com/sourceid/18200156711">Current month's CiteScore Tracker</a><br> H index (2018): <strong>21</strong></p> <p>We have more than 10,000 readers from South Korea to Nigeria.</p> <p><strong>Abstracted/Indexed in</strong><br>Academic Search Complete, Bangladesh Journals Online, Biological Abstracts, BIOSIS Previews, CAB Abstracts, Current Abstracts, <a href="http://bit.ly/2r4KLsU">Directory of Open Access Journals</a>, EMBASE/Excerpta Medica, Global Health, Google Scholar, HINARI (WHO), International Pharmaceutical Abstracts, Open J-gate, Science Citation Index Expanded, SCOPUS and Social Sciences Citation Index</p> <p><strong>Members</strong><br>Bangladesh Journal of Pharmacology is the member of <a href="https://oaspa.org/member/bangladesh-journal-of-pharmacology/">OASPA</a> (Open Access Scholarly Publishers Association), <a href="http://publicationethics.org/">COPE</a> (Committee on Publication Ethics), The International Society of Managing and Technical Editors (<a href="http://www.ismte.org/members/">ISMTE</a>) and Asian Council of Science Editors.</p> <h1 style="color: red;">Our activities are slow due to COVID-19 Lockdown</h1>Bangladesh Pharmacological Societyen-USBangladesh Journal of Pharmacology1991-0088<p>Authors who publish with this journal agree to the following terms:</p> <ol> <li class="show">Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a <a href="http://creativecommons.org/licenses/by/4.0/" target="_new"><span style="color: #337755;">Creative Commons Attribution License</span></a> that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.</li> <li class="show">Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.</li> <li class="show">Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See <a href="http://opcit.eprints.org/oacitation-biblio.html" target="_new"><span style="color: #337755;">The Effect of Open Access</span></a>).</li> </ol>Efficacy of beta-blockers in the treatment of sepsis
https://www.banglajol.info:443/index.php/BJP/article/view/46001
<p>This meta-analysis is to systematically evaluate the efficacy and safety of beta-blockers in the treatment of sepsis. A total of 17 articles that met the inclusion criteria were included, and 10,385 cases were obtained. The meta-analysis results showed that patients with sepsis with beta-blocker usage had a significantly lower 28-day mortality. The heart rate decreased over time in patients with sepsis using beta-blocker. Moreover, central venous blood oxygen saturation increased after 24, 48, 72 hours of treatment; lactic acid and cardiac troponin I decreased after 48, 72 hours of treatment; and tumor necrosis factor-α, interleukin-1β levels decreased significantly after 12, 24, 48, 72 hours of treatment (p<0.05). In conclusion, beta-blockers reduce 28-day mortality and heart rate.</p>Peng JinTao ZhaoYueyue WeiFang Zhao
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2021-01-032021-01-0316111810.3329/bjp.v16i1.46001Expression of HOXC10 gene regulates the growth and invasion of prostate cancer cells
https://www.banglajol.info:443/index.php/BJP/article/view/50244
<p>The present study was undertaken to decipher the role of HOXC10 gene in regulating the growth and metastasis of prostate cancer. The results revealed significant (p<0.05) up-regulation of HOXC10 gene in human prostate cancer tissues and cell lines. The silencing of HOXC10 transcript level significantly (p<0.05) inhibited the growth and colony formation of DU145 and 22Rv1 prostate cancer cells. The DAPI staining revealed that inhibition of DU145 and 22Rv1 prostate cancer cell viability was due to the induction of apoptosis. The transwell assay showed that HOXC10 significantly (p<0.05) inhibits the invasion of prostate cancer cells. The Western blotting revealed that HOXC10 gene exerts its effects via modulation of Ras/Raf/MEK/ERK signaling cascade. Collectively, the results point towards the therapeutic potential of HOXC10 in the treatment of prostate cancer.</p>Hongmei SongXuxiao YeTao LiangDongliang YanZuowei Li
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http://creativecommons.org/licenses/by/4.0
2021-01-042021-01-04161192610.3329/bjp.v16i1.50244Bufalin inhibits the growth and epithelial to mesenchymal transition of human gastric cancer cells via modulation of MEK/ERK pathway
https://www.banglajol.info:443/index.php/BJP/article/view/50548
<p>This study was designed to evaluate the anti-cancer effects of bufalin against the human gastric cancer cells and unveil the underlying mechanism. The results showed that bufalin inhibited the proliferation and colony formation of the MGC-803 gastric cancer cells and exhibited an IC<sub>50</sub> of 10 μM. These antiproliferative effects were found to be due to the induction of G<sub>2</sub>/M cell cycle arrest. The G<sub>2</sub>/M cell cycle arrest was also concomitant with inhibition of cdc2, cdc25 and cyclin B1. Furthermore, bufalin suppressed the epithelial-to-mesenchymal transition, migration, and invasion of the MGC-803 gastric cancer cells. The Western blot analysis revealed that bufalin exerted its effects via deactivation of EK/ERK signaling pathway. Taken together, these results suggest the potential of bufalin as the lead molecule for the development of chemotherapy for gastric cancer. </p>Yi ZhouLiguo WangHui LinYunxia WangKezhu Hou
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2021-01-052021-01-05161273310.3329/bjp.v16i1.50548