<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Saugi Abduh</style></author><author><style face="normal" font="default" size="100%">Purwanto Bambang</style></author><author><style face="normal" font="default" size="100%">Dirgahayu Paramasari</style></author><author><style face="normal" font="default" size="100%">Soetrisno</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cardioprotective Effects of Thymoquinone on Myocardial Fibrosis</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cardiac Fibrosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipopolysaccharide</style></keyword><keyword><style  face="normal" font="default" size="100%">Nigella sativa</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative stress.</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2023</style></year><pub-dates><date><style  face="normal" font="default" size="100%">October 2023</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">15</style></volume><pages><style face="normal" font="default" size="100%">924-927</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Introduction:&lt;/strong&gt; Thymoquinone (TQ) is one of the active ingredients in herbal plants such as &lt;em&gt;Nigella sativa &lt;/em&gt;which has antioxidant and anti-inflammatory properties thus may inhibits cardiac fibrosis formation. This study aims to determine the effectiveness of Thymoquinone as a cardioprotective agent in suppressing the extent of fibrosis in Wistar rats induced with lipopolysaccharide (LPS). &lt;strong&gt;Methods&lt;/strong&gt;: This post-test only control study used 30 Wistar rats which were divided into 5 groups: saline, LPS-induced cardiac fibrosis, LPS-induced cardiac fibrosis treated with TQ 10 mg/mL, LPS-induced cardiac fibrosis treated with TQ 20 mg/mL, and LPS-induced cardiac fibrosis treated with TQ 40 mg/mL. Serum IL-6, GSH, and cTnT levels were measured using ELISA, and Mason's trichrome staining was used to assess myocardial fibrosis. &lt;strong&gt;Results:&lt;/strong&gt; The LPS10+TQ20 and LPS10+TQ40 groups exhibited significantly lower levels of IL-6 compared to the LPS10+TQ10 group (p &amp;lt; 0.05). GSH levels did not show a significant decrease in the TQ groups across different doses (p=0.771). The TQ-treated group demonstrated lower cTnT levels compared to the LPS-only group (p&amp;lt;0.05). Thymoquinone treatment resulted in reduced fibrosis area compared to the LPS10 group (p&amp;lt;0.05). &lt;strong&gt;Conclusions: &lt;/strong&gt;TQ has a promising cardioprotective effect on the formation of cardiac fibrosis in Wistar rats induced with LPS.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><work-type><style face="normal" font="default" size="100%">Research Article</style></work-type><section><style face="normal" font="default" size="100%">924</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Saugi Abduh&lt;sup&gt;1,2,*&lt;/sup&gt;, Purwanto Bambang&lt;sup&gt;3&lt;/sup&gt;, Dirgahayu Paramasari&lt;sup&gt;4&lt;/sup&gt;, Soetrisno&lt;sup&gt;5&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Doctoral Student in Medical Science, Faculty of Medicine, Sebelas Maret University, Surakarta, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;2&lt;/sup&gt;Division of Cardiology, Department of Internal Medicine, Sultan Agung Islamic University, Semarang, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;3&lt;/sup&gt;Division of Nephrology and Hypertension, Department of Internal Medicine, Sebelas Maret University, Surakarta, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;4&lt;/sup&gt;Department of Parasitology, Sebelas Maret University, Surakarta, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;5&lt;/sup&gt;Department of Obstetrics and Gynecology, Sebelas Maret University, Surakarta, INDONESIA.&lt;/p&gt;
</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Melva Louisa</style></author><author><style face="normal" font="default" size="100%">Meuthia Faralita Annisa</style></author><author><style face="normal" font="default" size="100%">Pamela Basuki</style></author><author><style face="normal" font="default" size="100%">Brigitta Cindy Lauren</style></author><author><style face="normal" font="default" size="100%">Syarinta Adenina</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Alpha-Mangostin Enhances Proliferation in Sorafenib-Surviving HepG2 Liver Cancer Cells by Increasing Anti-Apoptosis and Antioxidant Markers Expressions</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Anti-cancer drug resistance</style></keyword><keyword><style  face="normal" font="default" size="100%">Caspase</style></keyword><keyword><style  face="normal" font="default" size="100%">Hepatocellular carcinoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Ki-67</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative stress.</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2022</style></year><pub-dates><date><style  face="normal" font="default" size="100%">June 2022</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">14</style></volume><pages><style face="normal" font="default" size="100%">584-590</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Background:&lt;/strong&gt; Sorafenib is the first-line systemic option for treatment in advanced liver cancer. However, sorafenib resistance may develop rapidly, which may involve apoptosis and oxidative stress dysregulations. Several alternative treatments have been suggested to alleviate the delayed resistance of cancer cells to sorafenib, including alpha mangostin (AM). According to an earlier study, AM might be able to overcome doxorubicin resistance in hepatocellular cancer cells. &lt;strong&gt;Objective:&lt;/strong&gt; The aim of this study was to investigate the effects of AM in sorafenib-surviving HepG2 cells, a hepatocellular carcinoma (HCC) cell line. &lt;strong&gt;Methods:&lt;/strong&gt; Sorafenib 10 μM was used to treat HepG2 to obtain sorafenib-surviving cells. Subsequently, sorafenib surviving cells were treated with DMSO -(vehicle) or sorafenib (SF) 10 μM or AM 20 μM, or SF 10 μM + AM 20 μM. Afterward, the cells were counted, collected and extracted for RNA. The mRNA expressions of Ki-67, c-Jun, Bcl-2, Bax, Caspase-3 and -9, GPx, and MnSOD were then quantified using qRT-PCR.&lt;strong&gt; Results&lt;/strong&gt;: Treatment of alpha-mangostin, alone or in combination with sorafenib combined enhanced the expressions of proliferation markers, Ki-67 and c-Jun. In addition, there was a marked increase in mRNA expressions of Bax and BCl2, but not Caspase-3 and -9. There were amplifications of antioxidant markers expressions, GPx, and MnSOD after AM or a combination of sorafenib and AM.&lt;strong&gt; Conclusion:&lt;/strong&gt; Treatment of alpha mangostin in sorafenib-surviving HCC cells caused an increase in proliferation markers, which might be explained by the reduced expressions of apoptosis markers and enhancement of antioxidant markers.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><work-type><style face="normal" font="default" size="100%">Research Article</style></work-type><accession-num><style face="normal" font="default" size="100%">15</style></accession-num><section><style face="normal" font="default" size="100%">584</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Melva Louisa&lt;sup&gt;1,*&lt;/sup&gt;, Meuthia Faralita Annisa&lt;sup&gt;2&lt;/sup&gt;, Pamela Basuki&lt;sup&gt;2&lt;/sup&gt;, Brigitta Cindy Lauren&lt;sup&gt;2&lt;/sup&gt;, Syarinta Adenina&lt;sup&gt;3&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Department of Pharmacology and Therapeutics, Faculty of Medicine, Universitas Indonesia, Jakarta, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;2&lt;/sup&gt;Medical student, Faculty of Medicine Universitas Indonesia, Jakarta, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;3&lt;/sup&gt;Department of Pharmacology, Faculty of Medicine, YARSI University, Jakarta, INDONESIA.&lt;/p&gt;
</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Agung Saprasetya Dwi Laksana</style></author><author><style face="normal" font="default" size="100%">Harianto Notopuro</style></author><author><style face="normal" font="default" size="100%">Arifa Mustika</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Ameliorative Effects of Moringa (Moringa Oleifera Lam.) Leaves Extract on Lead-Induced Oxidative Stress, Hepcidin and δ-Alad Levels in Rat’s Blood</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Blood</style></keyword><keyword><style  face="normal" font="default" size="100%">Hepcidin</style></keyword><keyword><style  face="normal" font="default" size="100%">Lead poisoning</style></keyword><keyword><style  face="normal" font="default" size="100%">Moringa</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative stress.</style></keyword><keyword><style  face="normal" font="default" size="100%">δ-ALAD</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2022</style></year><pub-dates><date><style  face="normal" font="default" size="100%">December 2022</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">14</style></volume><pages><style face="normal" font="default" size="100%">856-862</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Lead (Pb) is a toxic heavy metal that cause a lot health problem. Blood, especially hemoglobin and erythrocyte, is the main target of lead poisoning. Literatures explain that moringa has phytochemical contents to reduce heavy metal poisoning. This study aimed to examine ameliorative effects of moringa leaves extract on oxidative stress, hepcidin increasement and δ-alad level decline induced by lead poisoning in the blood of rat model. &lt;strong&gt;Methods: &lt;/strong&gt;This study was completely randomized posttest-control group design. Forty-eight males Rattus norvegicus Wistar strain rat were divided into 4 groups. The control group or G0 (given Pb orally doses of 750 mg/kgBW/day for 7 days and was not given 50% ethanol extract of moringa leaves/MLEE). Three treatment groups (G1, G2 and G3), all were given Pb at a dose of 750 mg/kgBW/day orally for 7 days, followed by administration of MLEE for 14 days at a dose of 250 mg/kgBW/day, 500 mg/kgBW/day and 1,000 mg/kg/day orally, respectively. Blood samples were taken one day after 14 days of MLEE treatment. Pb levels was examined by AAS and δ-ALAD levels, GSH levels, MDA levels and hepcidin levels examined by ELISA.&lt;strong&gt; Results:&lt;/strong&gt; MLEE doses 1,000 mg/kgBW/day for 14 days increased δ-ALAD levels, GSH levels, hepcidin levels and reduce MDA levels significantly compared to the control group. &lt;strong&gt;Conclusion:&lt;/strong&gt; Moringa leaves ameliorate lead-induced poisoning by reducing oxidative stress, declining hepcidin, and increasing δ-ALAD in the blood of male Rattus norvegicus Wistar strains rats. Moringa leaves is beneficial to address Pb poisoning in the blood through antioxidants, anti-inflammation, and improving δ-ALAD level in the blood of Wistar strain rats.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><work-type><style face="normal" font="default" size="100%">Research Article </style></work-type><section><style face="normal" font="default" size="100%">856</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Agung Saprasetya Dwi Laksana&lt;sup&gt;1,2&lt;/sup&gt;, Harianto Notopuro&lt;sup&gt;3&lt;/sup&gt;, Arifa Mustika&lt;sup&gt;4,*&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Doctoral Program of Medical Science, Faculty of Medicine, Universitas Airlangga, Jl. Mayjen Prof. Dr. Moestopo 47 Surabaya 60131, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;2&lt;/sup&gt;Faculty of Medicine, Jenderal Soedirman University, Jl. Dr. Gumbreg No.1, Mersi, Purwokerto 53112, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;3&lt;/sup&gt;Department of Physiology and Biochemistry, Faculty of Medicine, Universitas Airlangga, Jl. Mayjen Prof. Dr. Moestopo 47 Surabaya 60131, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;4&lt;/sup&gt;Department of Anatomy, Histology, and Pharmacology, Faculty of Medicine, Universitas Airlangga, Jl. Mayjen Prof. Dr. Moestopo 47 Surabaya 60131, INDONESIA.&lt;/p&gt;
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