bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chlorobenzoxime inhibits respiratory syncytial virus infection in neonatal rats via up-regulation of IFN-γ in dendritic cells
Authors: Li Junzhao , Zhang Yonghai , Qiao Hongmei , Jin Yingji , Wang Jianmin , Yao Binghua 
Published: June 2020

Purpose: To investigate the effect of chlorobenzoxime on respiratory syncytial virus (RSV) infection in vitro in lung alveolar cells and in vivo in neonatal rats, as well as the mechanism of action involved.
Methods: RSV infection in neonatal rats was induced via intranasal administration of 2 x 106PFU viral particles. Reverse transcriptase-polymerase chain reaction (RT-PCR) and western blotting were used for determination of changes in interleukin expression.
Results: RSV infection in BEAS-2B cells caused significant reduction in viability and marked alteration in morphological appearance (p < 0.05). Exposure of RSV-infected BEAS-2B cells to chlorobenzoxime prevented viability reduction and changes in morphology, and led to reductions in RSV-mediated increases in levels of interleukin-6 and interleukin-8. Moreover, RSV infection significantly enhanced ROS levels in BEAS-2B cells, when compared to control cells (p < 0.05). Chlorobenzoxime at a concentration of 30 μM completely suppressed RSV-mediated generation of ROS in BEAS-2B cells. In neonatal rats, RSV-induced upregulation of interleukin-4, interleukin-13 and TNF-α, were suppressed in bronchoalveolar lavage fluid (BALF) and lung tissues by chlorobenzoxime. Moreover, the RSVmediated reduction in IFN-γ was maximally blocked by chlorobenzoxime at a dose of 10 mg/mL. Chlorobenzoxime enhanced the proportion of IFN-γ -producing cells in neonatal rat BALF.
Conclusion: Chlorobenzoxime exhibits antiviral against RSV infection in neonatal rats via increase in dendritic cell population, leading to inhibition of cytokine production. Therefore, chlorobenzoxime is a potential therapeutic agent for RSV infection.
Keywords: Respiratory syncytial virus, Cytokines, Dendritic cells, Lung aveolar cells, Morphology, Interleukins
Evaluation of chidamide and PFI-1 as a combination therapy for triple-negative breast cancer
Authors: Lin Nong , Yang Qiaolu , Xu Tong , Shi Lianguo 
Published: June 2020

Purpose: To evaluate the in vitro and in vivo effects of the combination therapy of histone deacetylases (HDAsC) inhibitor, chidamide, and bromodomain-containing proteins (BETs) inhibitor, PFI-1, on triplenegative breast cancer (TNBC).
Methods: Four distinct breast cancer cell lines and one TNBC mouse model were treated with vehicle, chidamide, PFI-1 alone, or chidamide and PFI-1. The inhibitory effect of chidamide or PFI-1 on HDACs and BETs was assessed by HDAC enzyme inhibition and AlphaScreen assays. Cell viability was determined by MTT assay while protein expression of p-STAT3 was evaluated by western blotting and immunohistochemistry (IHC) staining assay.
Results: Chidamide exerted inhibitory effect on HDACs while PFI-1 inhibited BET proteins. The threedimensional model demonstrated the interactions between chidamide and HDAC2, and between PFI-1 and BRD4. Chidamide or PFI-1 exerted inhibitory effects on breast cancer cell proliferation in vitro. However, the combination of PFI-1 and chidamide significantly inhibit MDA-MB-231 cell viability, and decrease the expression of p-STAT3, when compared to that treated with chidamide or PFI-1 alone. Moreover, the combined inhibitory effect of PFI-1 and chidamide on tumor growth was also found in the in vivo mice experiments.
Conclusion: The combination of chidamide and PFI-1 is a potential is a potential therapeutic strategy for the management of TNBC.
Keywords: Triple-negative breast cancer, Histone deacetylases, Bromodomain
Evaluation of super-disintegrant potential of acid-modified starch derived from <i>Borassus aethiopum</i> (Aracaceae) shoot in paracetamol tablet formulations
Authors: Azubuike Chukwuemeka P. , Ubani-Ukoma Uloma N. , Afolabi Abiola R. , Cardoso-Daodu Ibilola M. 
Published: June 2020

Purpose: To evaluate the super-disintegrant potentials of acid modified Borassus aethiopum starch (AMS) in comparison with native starch (NS) and commercial disintegrant sodium starch glycolate (SSG).
Methods: Compatibility of AMS with paracetamol powder was evaluated using Fourier transform infrared (FTIR) spectrophotometry. Seven batches of paracetamol granules and tablets were prepared by wet granulation. AMS and NS were employed as disintegrants at concentrations of 2.43, 4.86 and 9.72 %w/w, respectively while 4.86 %w/w SSG was used as standard disintegrant. All the batches of the granules were compressed under the same compression settings. The properties of the granules as well as those of the tablets were assessed.
Results: AMS was compatible with paracetamol powder as no noticeable interaction was observed in FTIR study. The paracetamol tablets formulated using AMS as disintegrant demonstrated satisfactory friability, weight uniformity, hardness, and superior disintegration characteristics to the formulations containing NS and SSG as disintegrant. Even at a lower concentration (2.43 %w/w), AMS possessed better disintegrant property than NS and SSG. AMS and NS had dimensionless disintegrant quantity of 1.447 and 0.005, respectively. As expected, increase in AMS concentration showed a decrease in disintegration time.
Conclusion: AMS could be a potential low-cost super-disintegrant in formulation of paracetamol tablets.
Keywords: Acid modified starch, Borassus aethiopum, Disintegrant, Compatibility
Protective effect of astragalus injection against myocardial injury in septic young rats via inhibition of JAK/STAT signal pathway and regulation of inflammation
Authors: Zhao Zhihong , Wang Xuejing , Li Xiumin , Li Hongshuang , Xu Bin 
Published: June 2020

Purpose: To investigate the protective effect of astragalus injection against myocardial injury in septic young rats, and the underlying mechanism of action.
Methods: Seventy-two healthy Sprague Dawley (SD) rats were randomly selected and used to establish a young rat model of sepsis. The young rats were randomly divided into 3 groups: sham, model and astragalus injection groups. Each group had 24 young rats. Serum cardiac troponin I (cTnI), IL-10, IL-6, JAK2 and STAT3 were measured after op.
Results: Compared with sham group, serum cTnI level in the model group was significantly higher, while serum cTnI level of the drug group was significantly lower than that of the model group (p < 0.05). Compared with model group, the level of IL-10 in the myocardial tissue of the drug group was significantly elevated, while IL-6 level was lower (p < 0.05). Relative to sham rats, myocardial JAK2 and STAT3 protein levels in model rats were high. However, myocardial JAK2 and STAT3 proteins in the drug-treated rats were significantly downregulated, relative to model rats (p < 0.05).
Conclusion: Astragalus injection upregulates IL-10 and IL-6 in rats by inhibiting the activation of JAK/STAT signal pathway, and via maintenance of pro-inflammation/anti-inflammation balance. Thus, astragalus exerts protective effect against myocardial injury in sepsis, and can potentially be developed for use as such in clinical practice.
Keywords: Astragalus injection, JAK/STAT signal pathway, Pro-inflammatory/anti-inflammatory imbalance, Sepsis, Myocardial injury
Cytotoxic effect of acetogenins and sesquiterpenes obtained from the Red alga <i>Laurencia majuscula</i>
Authors: Alorfi Hajer S. , Ghandourah Mohamed A. , Turki Adnan J. 
Published: June 2020

Purpose: To evaluate the cytotoxicity of n-hexane extract and its metabolites obtained from the red alga, Laurencia majuscula, against three cancer cell lines HCT-116 (colon cancer), PC-3 (prostate cancer) and HepG2 (liver cancer) cells; and to identify the phytochemical compound(s) involved.
Methods: Solvent extraction, thin layer chromatography, aluminum oxide column chromatography, and preparative thin layer chromatography (PTLC) were employed for isolating pure compounds from nhexane extract of Laurencia majuscula. Nuclear magnetic resonance (NMR) and mass spectrometry (MS) measurements were used for structural elucidation of the compounds. The cytotoxicity of the nonpolar extract and isolated compounds were evaluated against HCT, PC-3, and HepG2 cells using MTT assay, relative to the standard cytotoxic drug (cisplatin).
Results: Three sesquiterpenes (1, 2 and 8), and five acetogenins (3-7) were isolated from the n-hexane extract. The n-hexane extract showed higher potent cytotoxic effect than sesquiterpenes and the acetogenins (3-7).
Conclusion: These results indicate that the n-hexane extract of Laurencia majuscula exerts significant cytotoxicity against HCT-116, PC-3 and HepG2 cell lines, thus suggesting that the plant extract may be effective chemotherapeutic agents for the management of colon, postrate and liver cancer.
Keywords: Red Sea alga, Rhodomelaceae, Polyketides, Terpenes, Anticancer
Effect of sodium dichloroacetate as single agent or in combination with cisplatin in normal and human cervical cancer cell lines
Authors: Zugasti Alejandro , Rivera Ana L. , Silva Sonia Y. , Alfaro Miguel A. , Sierra Crystel A. 
Published: June 2020

Purpose: To evaluate the synergistic cytotoxicity of sodium dichloroacetate (DCA) in combination with cisplatin (CIS) against human cervical cancer cell lines.
Methods: Cervical cancer SiHa and HeLa cells and normal cells (Hek-293, Vero, peripheral blood mononuclear and human erythrocytes) were treated in vitro with DCA and CIS individually or their combination. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method while hemolytic activity was evaluated from the released hemoglobin. Halfmaximal inhibitory concentration (IC50) of DCA or CIS was obtained.
Results: The combination of DCA + CIS decreased the cell viability of SiHa, Hek-293, Vero, and PBMC cells, but not of Hela cells (p < 0.05). Furthermore, the individual treatments alone or in combination did not cause significant hemolysis (p < 0.05).
Conclusion: The combination of DCA + CIS increases the damage caused by CIS alone on SiHa cells. It also decreases the cell viability of Hek-293 and Vero without affecting peripheral blood mononuclear and human erythrocyte integrity. The results suggest that the combination of DCA and CIS can induce synergistic antitumor effect in different types of cancer cell lines. However, further studies are required to determine the biological effects of the combination of DCA and CIS in vivo.
Keywords: Cervical cancer, Sodium dichloroacetate, Cisplatin, Viability, Hemolysis
Evaluation of 90-day subchronic oral toxicity of aqueous extract of <i>Gmelina arborea</i> Roxb (Verbenaceae) leaves in Wistar rats
Authors: Osseni Razack , Simon Azonbakin , Aboudoulatif Diallo , Ganfon Habib , Marius Adjagba , Kaossarath Fagbemi , Sekossounon Sanni , Awede Bonaventure , André Bigot , Raphaël Darboux , Anatole Lalèyè 
Published: June 2020

Purpose: To evaluate the 90 day sub-chronic toxicity of aqueous extract of Gmelina arborea leaves in Wistar rats.
Methods: Rats were submitted to repeated daily oral administration of extract (250, 62.5 and 15.62 mg/kg) of Gmelina arborea leaves. The control groups were given distilled water and the rats were monitored for any toxicity symptoms as well as body and organs weights, water and food intake changes. The biochemical, haematological and histolopathological parameters were analysed.
Results: The 90 days administration of the aqueous extract did not produce any toxicity signs or mortality. In addition, no significant alteration in water or food intake by the rats was observed. Although there were no changes in the body weights, significant decrease in the weight of the kidneys of the rats was observed at 250 mg/kg. Biological parameters as well as the histopathology of liver and kidneys were not significantly affected. Significant decreases were noted in glucose level at the three dose levels. In addition, significant difference in the levels of transaminases, glucose and platelets were observed.
Conclusion: The 90-days subchronic toxicity test on Gmelina arborea did not produce any toxic effects. This confirms the safety of the plant leaves by traditional medicine practitioners.
Keywords: Gmelina arborea, Subchronic toxicity, Wistars rats, Biological parameters
Positive effects of angiotensin-converting enzyme (ACE) inhibitor, captopril, on pentylenetetrazole-induced epileptic seizures in mice
Authors: Tastemur Yasar , Gumus Erkan , Ergul Merve , Ulu Mustafa , Akkaya Recep , Ozturk Aysegul , Taskiran Ahmet Sevki 
Published: June 2020

Purpose: To evaluate the effects of an angiotensin-converting enzyme (ACE) inhibitor, captopril, on pentylenetetrazole (PTZ)-induced seizures and post-seizure hippocampal injury.
Materials: Thirty-five male Balb-c mice weighing 30 - 33 g were divided into control, saline PTZ, s(erum physiologic 1 ml/kg as solvent), positive control (valproic acid 200 mg/kg), captopril (25 mg/kg/day for 7 days), and captopril (50 mg/kg/day for 7 days) groups. PTZ (60 mg/kg) was administered thirty minutes after medication administration to induce epileptic seizures. The animals were observed for 30 min to record Racine stages, the time of the first myoclonic jerk (FMJ), and the occurrence of the first generalized tonic-clonic seizure (GTCS). Cornu Ammonis (CA)1, CA2, CA3, and the dentate gyrus (DG) of the hippocampus underwent histopathological examinations. The levels of total oxidant status (TOS), oxidative stress markers (total antioxidant status, TAS), and oxidative stress index (OSI) were measured in the brain tissue.
Results: Compared to PTZ group, 25 mg/kg captopril decreased seizure scores and delayed FMJ and GTCS (p < 0.05). Histopathological assessment demonstrated that both 25 and 50 mg/kg captopril alleviated neuronal injury in CA1, CA2, CA3, and DG compared to PTZ (p < 0.05). Also, TOS and OSI levels in the brain tissue were reduced by both 25 and 50 mg/kg doses of captopril (p < 0.05).
Conclusion: Captopril favorably improves epileptic seizure parameters and acts against post-seizure neuronal injury in the hippocampus. Captopril may be a drug of choice in epileptic individuals with hypertension.
Keywords: Captopril, Angiotensin-converting enzyme, Epilepsy, Pentylenetetrazole, Neuronal damage
Genomic analysis of tyrosine hydroxylase gene sequence variations and its association with D-9- tetrahydrocannabinol dependence in addicts
Authors: Javed Maryam , Raza Ali , Nadeem Asif , Yaqub Tahir , Ahmed Muhammad Danish 
Published: June 2020

Purpose: To elucidate the genetic basis of drug addiction by conducting a genetic analysis of TH (tyrosine hydroxylase) gene and the novel polymorphisms that might help in understanding addiction and its molecular basis.
Methods: Forty-two subjects were recruited into three groups for this study. DNA was isolated from the individuals. PCR amplification of TH gene was carried out and amplicons were sequenced. Genomic characterization of TH gene provided five polymorphic loci – TH 1, TH 2, TH 3, TH 4 and TH 5 which were found among all the groups.
Results: According to Shannon’s diversity index, the studied population was between 0.0762 and 0.6032. Heterozygosity index depicted that TH 1 locus was less heterozygous (0.3288), followed by TH 5 (0.3152). TH 1 (0.1462) was the least heterozygous. Genotypic analysis predicted that among these five loci, TH 4 (p = 0.039898) and TH 2 (p = 0.851716) were non-significant (p > 0.05) and obeyed Hardy Weinberg Equilibrium (HWE) law. There are few genetic changes in the studied population that can statistically be associated with drug addiction. Still, their genotypic distribution in the gene pool was very low.
Conclusion: On the basis of these findings, drug addiction in the studied population is more likely a social issue rather than a genetic one.
Keywords: Tyrosine hydroxylase, SNP, Drug dependence
MiR-574-5p alleviates sepsis-induced acute lung injury by regulating TRAF6/NF-κB pathway
Authors: Xu Changfu , Chong Lei , Yu Gang , Zhang Hailin 
Published: June 2020

Purpose: To investigate the protective effect of miR-574-5p pretreatment against acute lung injury (ALI) induced by sepsis.Methods: A male C57BL/6 mouse model of sepsis-induced ALI was established by cecal ligation and puncture (CLP) and treated with miR-574-5p agomir (intravenous injection, 80 mg/kg per day, 3 days). After that, blood and lung samples were obtained for histopathological observation. Myeloperoxidase (MPO) activity, inflammatory cell infiltration, and cytokine expression were analyzed. The target gene of miR-574-5p was predicted using TargetScan prediction, and verified by luciferase assay and western blot.Results: In sepsis-induced ALI mice model, downregulation of miR-574-5p was observed. Pretreatment of miR-574-5p significantly alleviated ALI by suppressing histological damage, and reducing MPO activity and inflammatory cell infiltration, as well as decreasing cytokine expression. The underlying mechanism was that miR-574-5p targeted TNF receptor associated factor 6 (TRAF6) and suppressed the downstream NF-κB pathway. Moreover, TRAF6 overexpression reversed the effects of miR-574-5p on ALI.Conclusion: MiR-574-5p pretreatment suppresses inflammatory responses, thus reducing lung injury induced by sepsis in mice, partly via the regulation of TRAF6 and NF-κB pathway. Therefore, this approach can potentially be used for the clinical management of ALI in humans
Keywords: Sepsis, Acute lung injury, MiR-574-5p, TRAF6, NF-κB pathway
PSAT1 prompted cell proliferation and inhibited cell apoptosis in multiple myeloma through regulating PI3K/AKT pathway
Authors: Zhu Hongqing , Si Yejun , Zhuang Yun , Li Meng , Ji Jianmin , Ji Ou , Shen Qun 
Published: June 2020

Purpose: To identify the biological function of phosphoserine aminotransferase 1 (PSAT1) in regulating cell proliferation and apoptosis in multiple myeloma (MM).Methods: The mRNA and protein levels of PSAT1 were determined using quantitative real-time polymerase chain reaction (PCR) and western blotting, respectively. Cell proliferation was measured using CCK-8 assay.Results: PSAT1 mRNA and protein expression levels were significantly increased in MM cell lines when compared to control cells. Moreover, downregulation of PSAT1 inhibited MM cell proliferation and induced cell apoptosis, whereas overexpression of PSAT1 promoted MM cell proliferation and suppressed cell apoptosis. Further analysis demonstrated that the underlying mechanism was via regulation of PI3K/AKT pathway.Conclusion: The results identified a novel role for PSAT1 in the progression of MM, which may provide a therapeutic and a new anticancer target for the therapy of MM.
Keywords: Multiple myeloma, PSAT1, Cell proliferation, PI3K/AKT pathway
Picroside-I attenuated isoproterenol-induced heart damage via modification of cardio-morphology, infarct size and inflammatory cascade
Authors: Hao Yi , Cui Zhixiong , Zhang Shuang , Liu Tong 
Published: June 2020

Purpose: To study the effect of picroside-I (PIC-I) on isoproterenol (ISO)-induced heart damage in rats through determination of infarct size, antioxidant enzymes, cardiac/inflammatory and apoptotic markers, as well as cardio-morphology.Methods: A total of 32 rats were divided equally into 4 groups. Rats in normal control group were treated with saline only, while myocardial infarction (MI) rat model was prepared by intraperitoneal (i.p.) injection of ISO at a concentration of 100 mg/kg. Rats pretreated with PIC-Iat dose 10 mg/kg (i.p) for 28 days and administered with isoproterenol. Another group of rats was administered only with PIC-I (10 mg/kg) for 28 days.Results: After 28 days of pretreatment with PIC-I, there were significant increases in arterial blood pressure and cardiac antioxidants, as well as marked decreases in infarct size, cardiac markers, inflammatory markers and apoptotic markers in rats with ISO-induced heart damage, when compared with rats given ISO alone. Rats administered PIC-I showed better histology, with reduced necrosis and prominent cardiac fibers.Conclusion: PIC-1 pre-treatment for 28 days significantly reversed elevations in infarct size, cardiac/inflammatory and apoptotic markers, and also improved antioxidant status and cardiacmorphology in rats with ISO-induced heart damage.
Keywords: Picroside-I, Isoproterenol, Infarct size, Inflammation, Apoptosis
Effects of ginsenoside Rg3 on bone loss, bone mineral density and osteoclast number in glucocorticoid-induced osteoporosis rats, and the likely michanism of action
Authors: Peng Maoxiu , Jiang Gangyl , He Shaoqi , Tang Chengxuan 
Published: June 2020

Purpose: To investigate the effect of ginsenoside Rg3 on bone loss, bone mineral density (BMD) and osteoclast number in glucocorticoid-induced osteoporosis (GIOP) rats, and the mechanism of action involved.Methods: Sixty female Wistar rats were assigned to control, model group, ginsenoside Rg3, and alendronate sodium groups, comprised of 15 rats per group. The osteoporosis rat model was established via intramuscular injection of dexamethasone. Changes in bone mineral content (BMC), BMD trabecular thickness and area, osteoblasts and osteoclasts in femurs and lumbar vertebrae were measured after 3 months of treatment.Results: There were significantly higher BMC and BMD levels in ginsenoside Rg3 group than in alendronate rats (p < 0.05). The thickness and trabecular area in femur and lumbar vertebrae in the ginsenoside Rg3 group were significantly higher than those in the model group (p < 0.05), but were comparable with those in the alendronate sodium group (p > 0.05). There were marked increases in osteoblasts, and marked decreases in osteoclasts in the ginsenoside Rg3 group, alendronate sodium and control rats, relative to model rats (p < 0.05).Conclusion: Ginsenoside Rg3 arrests bone loss, and enhances bone density, trabecular thickness and area, bone microstructure, osteoblast activity and population of osteoclasts number in glucocorticoidinduced osteoporotic rats. This provides a new research direction for the clinical treatment ofosteoporosis.
Keywords: Ginseng soap, Rg3, Glucocorticoid, Osteoporosis, Bone loss, Bone mineral density, Osteoclast population
Chondrocyte proliferation is promoted by 7-H-pyrrolo[2,3- d]pyrimidine via up-regulation of type II collagen matrix
Authors: Chen Jinsong , Zhang Lin , Zhang Junwu 
Published: June 2020

Purpose: To investigate the effect of 7-H-pyrrolo[2,3-d]pyrimidine derivative (7-HPPD) on the viability of chondrocytes in vitro, and to elucidate the associated mechanisms.Methods: Chondrocyte proliferation was determined by 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay while cell cycle was assessed by flow cytometry. Western blot and immunohistochemical staining assays were used to determine protein levels.Results: The results show that 7-HPPD significantly increased the proliferation rate of chondrocytes in a concentration-dependent manner (p < 0.05). The proportion of chondrocytes in S phase increased significantly with subsequent reduction in G0/G1 phase of cell cycle on treatment with 7-HPPD (p <0.05). Thus, 7-HPPD increased the rate of chondrocyte proliferation by promoting transition through G1/S phase of cell cycle. Reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis revealed that treatment of chondrocytes with 7-HPPD caused a marked increase in the level of cyclin D1, cyclin dependent kinase (CDK)-4 and CDK6 proteins (p < 0.05). Western blot and immunohistochemical staining assays showed that 7-HPPD treatment caused a significant increase in the levels of type II collagen matrix in the chondrocytes.Conclusion: Proliferation of chondrocytes is increased by 7-HPPD and this occurs by facilitating G1/S phase transition and increasing expression of cyclin D1, CDK4 and CDK6 proteins. Therefore, 7-HPPD may be developed as a chemotherapeutic agent for the treatment of osteoarthritis.
Keywords: Immunohistochemistry, Type II collagen, G1/S phase, Cyclin D1, Osteoarthritis