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Ginsenoside Rc attenuates myocardial ischaemic injury through antioxidative and anti-inflammatory effects. 人参皂苷Rc通过抗氧化和抗炎作用减轻心肌缺血损伤。
IF 3.8 3区 医学
Pharmaceutical Biology Pub Date : 2022-12-01 DOI: 10.1080/13880209.2022.2072518
Lei Shi, Wenwen Fu, Huali Xu, Shihui Li, Xinyu Yang, Wei Yang, Dayun Sui, Quanwei Wang
{"title":"Ginsenoside Rc attenuates myocardial ischaemic injury through antioxidative and anti-inflammatory effects.","authors":"Lei Shi,&nbsp;Wenwen Fu,&nbsp;Huali Xu,&nbsp;Shihui Li,&nbsp;Xinyu Yang,&nbsp;Wei Yang,&nbsp;Dayun Sui,&nbsp;Quanwei Wang","doi":"10.1080/13880209.2022.2072518","DOIUrl":"https://doi.org/10.1080/13880209.2022.2072518","url":null,"abstract":"<p><strong>Context: </strong><i>Panax ginseng</i> C. A. Meyer (Araliaceae) is a famous Asian medicine. Ginsenoside Rc is a component isolated from <i>Panax ginseng</i>.</p><p><strong>Objective: </strong>This study evaluates the effect of ginsenoside Rc on myocardial ischaemic injury.</p><p><strong>Materials and methods: </strong>Male Swiss mice were subcutaneously injected with 50 mg/kg isoproterenol once a day for three days. Ginsenoside Rc (10, 20, or 40 mg/kg) was intragastrically administered 1 h after isoproterenol injection. The mice in the control group were subcutaneously injected with normal saline and intragastrically given 0.5% CMC-Na. CK-MB and troponin T were assayed. Histopathological examination of myocardium was conducted. The expression of Nrf2, GCLC, GCLM and HO-1 in heart tissues was evaluated by Western blot.</p><p><strong>Results: </strong>In myocardial ischaemic mice, ginsenoside Rc reduced the levels of CK-MB (197.1 ± 15.7, 189.9 ± 19.0, 184.0 ± 14.4 vs. 221.6 ± 27.9) and troponin T (10.3 ± 1.7, 9.5 ± 1.3, 8.7 ± 1.7 vs. 13.4 ± 2.4). Ginsenoside Rc attenuated the necrosis and inflammatory cells infiltration in myocardium. Furthermore, ginsenoside Rc not only decreased the contents of MDA, TNF-α but also increased GSH level in the heart tissues. The expression of Nrf2, GCLC, GCLM and HO-1 was significantly increased in the animals treated with ginsenoside Rc. ML385, an Nrf2 inhibitor, blocked partially the ginsenoside Rc-mediated cardioprotective effect. Ginsenoside Rc attenuated myocardial ischaemic injury in mice, which may be, in part, through its antioxidative and anti-inflammatory effects.</p><p><strong>Conclusions: </strong>This study indicated that ginsenoside Rc might be a novel candidate for treatment of myocardial ischaemia.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"60 1","pages":"1038-1046"},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9154762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10515492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 7
Veratramine ameliorates pain symptoms in rats with diabetic peripheral neuropathy by inhibiting activation of the SIGMAR1-NMDAR pathway. 维拉曲明通过抑制 SIGMAR1-NMDAR 通路的激活来改善糖尿病周围神经病变大鼠的疼痛症状。
IF 3.9 3区 医学
Pharmaceutical Biology Pub Date : 2022-12-01 DOI: 10.1080/13880209.2022.2136207
Yu Zhang, Guangyao Ye, Yuebo Chen, Chaoxu Sheng, Jianlin Wang, Lingsi Kong, Liyong Yuan, Chunyan Lin
{"title":"Veratramine ameliorates pain symptoms in rats with diabetic peripheral neuropathy by inhibiting activation of the SIGMAR1-NMDAR pathway.","authors":"Yu Zhang, Guangyao Ye, Yuebo Chen, Chaoxu Sheng, Jianlin Wang, Lingsi Kong, Liyong Yuan, Chunyan Lin","doi":"10.1080/13880209.2022.2136207","DOIUrl":"10.1080/13880209.2022.2136207","url":null,"abstract":"<p><strong>Context: </strong>Veratramine may have a potential therapeutic effect for diabetic peripheral neuropathy (DPN).</p><p><strong>Objective: </strong>To evaluate whether veratramine ameliorates neuropathic pain in a rat diabetic model.</p><p><strong>Materials and methods: </strong>Sprague-Dawley rats were used for a diabetic model induced by a streptozotocin + high-fat diet. Two months after the induction of the diabetic model, the rats with DPN were screened according to the mechanical pain threshold. The rats with DPN were divided into a model group (n = 12) and a treated group (n = 12). Rats with diabetes, but without peripheral neuropathy, were used in the vehicle group (n = 9). The treatment group received 50 μg/kg veratramine via the tail vein once a day for 4 weeks. During modelling and treatment, rats in all three groups were fed a high-fat diet.</p><p><strong>Results: </strong>The mechanical withdrawal threshold increased from 7.5 ± 1.9 N to 17.9 ± 2.6 N in DPN rats treated with veratramine. The tolerance time of the treated group to hot and cold ectopic pain increased from 11.8 ± 4.2 s and 3.4 ± 0.8 s to 20.4 ± 4.1 s and 5.9 ± 1.7 s, respectively. Veratramine effectively alleviated L4-L5 spinal cord and sciatic nerve pathological injury. Veratramine inhibited the expression of SIGMAR1 and the phosphorylation of the N-methyl-d-aspartate receptor (NMDAR) Ser896 site in spinal cord tissue, as well as inhibited the formation of SIGMAR1-NMDAR and NMDAR-CaMKII complexes.</p><p><strong>Discussion and conclusions: </strong>Veratramine may alleviate the occurrence of pain symptoms in rats with DPN by inhibiting activation of the SIGMAR1-NMDAR pathway.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"60 1","pages":"2145-2154"},"PeriodicalIF":3.9,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9665081/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10409637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cinobufagin induces acute promyelocytic leukaemia cell apoptosis and PML-RARA degradation in a caspase-dependent manner by inhibiting the β-catenin signalling pathway. Cinobufagin通过抑制β-catenin信号通路,以caspase依赖的方式诱导急性早幼粒细胞白血病细胞凋亡和PML-RARA降解。
IF 3.8 3区 医学
Pharmaceutical Biology Pub Date : 2022-12-01 DOI: 10.1080/13880209.2022.2118792
Yaoyao Bian, Mei Xue, Xinlong Guo, Wenjuan Jiang, Ye Zhao, Zhaofeng Zhang, Xian Wang, Yongkang Hu, Qi Zhang, Wenliang Dun, Liang Zhang
{"title":"Cinobufagin induces acute promyelocytic leukaemia cell apoptosis and PML-RARA degradation in a caspase-dependent manner by inhibiting the β-catenin signalling pathway.","authors":"Yaoyao Bian,&nbsp;Mei Xue,&nbsp;Xinlong Guo,&nbsp;Wenjuan Jiang,&nbsp;Ye Zhao,&nbsp;Zhaofeng Zhang,&nbsp;Xian Wang,&nbsp;Yongkang Hu,&nbsp;Qi Zhang,&nbsp;Wenliang Dun,&nbsp;Liang Zhang","doi":"10.1080/13880209.2022.2118792","DOIUrl":"https://doi.org/10.1080/13880209.2022.2118792","url":null,"abstract":"<p><strong>Context: </strong>Acute promyelocytic leukaemia (APL) is a malignant hematological tumour characterized by the presence of promyelocytic leukaemia-retinoic acid receptor A (PML-RARA) fusion protein. Cinobufagin (CBG) is one of the main effective components of toad venom with antitumor properties. However, only a few reports regarding the CBG treatment of APL are available.</p><p><strong>Objective: </strong>We explored the effect and mechanism of action of CBG on NB4 and NB4-R1 cells.</p><p><strong>Materials and methods: </strong>We evaluated the viability of NB4 and NB4-R1 cells treated with 0, 20, 40, and 60 nM CBG for 12, 24, and 48 h. After treatment with CBG for 24 h, Bcl-2 associated X (Bax), B-cell lymphoma 2 (Bcl-2), β-catenin, cyclin D1, and c-myc expression was detected using western blotting and real-time polymerase chain reaction. Caspase-3 and PML-RARA expression levels were detected using western blotting.</p><p><strong>Results: </strong>CBG inhibited the viability of NB4 and NB4-R1 cells. The IC<sub>50</sub> values of NB4 and NB4-R1 cells treated with CBG for 24 h were 45.2 nM and 37.9 nM, respectively. CBG induced NB4 and NB4-R1 cell apoptosis and PML-RARA degradation in a caspase-dependent manner and inhibited the β-catenin signalling pathway.</p><p><strong>Discussion and conclusion: </strong>CBG induced NB4 and NB4-R1 cell apoptosis and PML-RARA degradation in a caspase-dependent manner by inhibiting the β-catenin signalling pathway. This study proposes a novel treatment strategy for patients with APL, particularly those with ATRA-resistant APL.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"60 1","pages":"1801-1811"},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9518602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10417523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Fraxinol attenuates LPS-induced acute lung injury by equilibrating ACE-Ang II-AT1R and ACE2-Ang (1-7)-Mas and inhibiting NLRP3. 黄曲醇通过平衡ACE-Ang II-AT1R和ACE2-Ang (1-7)-Mas,抑制NLRP3,减轻lps诱导的急性肺损伤。
IF 3.8 3区 医学
Pharmaceutical Biology Pub Date : 2022-12-01 DOI: 10.1080/13880209.2022.2067571
Yan Wu, Xin Yang, Yuanyuan Ju, Fei Zhao
{"title":"Fraxinol attenuates LPS-induced acute lung injury by equilibrating ACE-Ang II-AT1R and ACE2-Ang (1-7)-Mas and inhibiting NLRP3.","authors":"Yan Wu,&nbsp;Xin Yang,&nbsp;Yuanyuan Ju,&nbsp;Fei Zhao","doi":"10.1080/13880209.2022.2067571","DOIUrl":"https://doi.org/10.1080/13880209.2022.2067571","url":null,"abstract":"<p><strong>Context: </strong>Acute lung injury (ALI) is a serious heterogenous pulmonary disorder. Fraxinol was selected for this study since it is a simple coumarin compound, not previously investigated in ALI.</p><p><strong>Objectives: </strong>This study investigates the ALI therapeutic effect and mechanisms of fraxinol.</p><p><strong>Materials and methods: </strong>Male BALB/c mice were treated with fraxinol (20, 40, and 80 mg/kg) following intranasal injection of lipopolysaccharide (LPS; 10 μg in 50 μL). The mice in control group were intratracheally injected with 50 μL phosphate buffered saline (PBS). Raw264.7 cells were treated with fraxinol by 100 ng/mL LPS for 6 h, then treated by different concentrations of fraxinol (5, 10, and 25 μM) for 48 h. Cells in control group were treated with PBS.</p><p><strong>Results: </strong>Fraxinol with doses of 20, 40, and 80 mg/kg significantly attenuated LPS-induced lung injury in mice (lung injury score, 10.4, 31.2, 50.3%). Fraxinol attenuated the apoptosis and nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing-3 (NLRP3) activation induced by LPS (apoptosis, 18.3, 30.2, 55.6%; NLRP3, 30.0, 47.7, 63.6%). The anti-apoptosis and anti-inflammation effects of fraxinol were also confirmed in Raw264.7 cells (apoptosis, 38.8, 55.3, 68.9%; NLRP3, 20.6, 55.7, 73.9%).</p><p><strong>Discussion and conclusion: </strong>The anti-ALI effects of fraxinol maybe by equilibrating ACE-Ang II-AT1R and ACE2-Ang (1-7)-Mas axis and inhibiting NLRP3 inflammasome. Our research provides a candidate drug in the treatment of ALI.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"60 1","pages":"979-989"},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9122403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10792755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Flaxseed extract reduces tissue accumulation and enhances urinary excretion of chondroitin sulphate in the rat: a possible new path in substrate reduction therapy for mucopolysaccharidosis. 亚麻籽提取物减少大鼠组织积累和增加硫酸软骨素尿排泄:一个可能的底物减少治疗粘多糖病的新途径。
IF 3.8 3区 医学
Pharmaceutical Biology Pub Date : 2022-12-01 DOI: 10.1080/13880209.2022.2068618
Sabir Es-Said, Karima Lafhal, Abdelaati Elkhiat, Miloud Hammoud, Noureddine Regbaoui, Aicha Ezoubeiri, Rachida Makbal, Safia Sbyea, Omar Elhiba, Souad Sellami, Hanane Rais, Abdallah Karim, Halima Gamrani, Noureddine Rada, Mohammed Bouskraoui, Naima Fdil
{"title":"Flaxseed extract reduces tissue accumulation and enhances urinary excretion of chondroitin sulphate in the rat: a possible new path in substrate reduction therapy for mucopolysaccharidosis.","authors":"Sabir Es-Said,&nbsp;Karima Lafhal,&nbsp;Abdelaati Elkhiat,&nbsp;Miloud Hammoud,&nbsp;Noureddine Regbaoui,&nbsp;Aicha Ezoubeiri,&nbsp;Rachida Makbal,&nbsp;Safia Sbyea,&nbsp;Omar Elhiba,&nbsp;Souad Sellami,&nbsp;Hanane Rais,&nbsp;Abdallah Karim,&nbsp;Halima Gamrani,&nbsp;Noureddine Rada,&nbsp;Mohammed Bouskraoui,&nbsp;Naima Fdil","doi":"10.1080/13880209.2022.2068618","DOIUrl":"https://doi.org/10.1080/13880209.2022.2068618","url":null,"abstract":"<p><strong>Context: </strong>Chondroitin 6 sulphate (C6S) is a glycosaminoglycan (GAG) whose accumulation is notable in mucopolysaccharidosis type IVA and VII. Flaxseed, <i>Linum usitatissimum</i> L. (Linaceae) (FS), is reported to have comparable properties to those of soybean, a source of genistein, a potential new treatment for MPSs.</p><p><strong>Objective: </strong>We assess the effect of total ethanol flaxseed extract (EFSE) in an animal model of C6S accumulation.</p><p><strong>Materials and methods: </strong>The study was performed in adult male Wistar rats (<i>n</i> = 24) for 15 successive days. The animals were divided into four groups: (1) control injected with physiological saline buffer, (2) intoxicated rats injected intraperitoneally with C6S, (3) intoxicated with C6S and treated with EFSE, and (4) treated with EFSE. All groups were subjected to histopathological and biochemical studies. The antioxidant and phytochemical properties of EFSE were examined.</p><p><strong>Results: </strong>Dry EFSE contains total phenols (6.28 mg EAG/g), condensed tannins (2.98 mg ECAT/g) and flavonoids (0.44 mg ECAT/g) with high antioxidant potential [RPE (IC<sub>50</sub> = 8.37 ± 0.176), DPPH (IC<sub>50</sub> = 12.79 ± 0.273)]. The LD<sub>50</sub> is higher than 5000 mg/kg. The histopathological examination showed an accumulation of C6S in the C6S intoxicated group, which disappeared in the C6S-EFSE treated group. GAGs assays showed an increased excretion in the C6S intoxicated group and increased excretion of 14% in the C6S-EFSE group compared to the C6S group.</p><p><strong>Discussion and conclusions: </strong>EFSE showed significant potential for chelation. Its use for the treatment of GAG accumulation could be suggested and generalized to a larger study population.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"60 1","pages":"879-888"},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9477488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10509070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Camel milk protein hydrosylate alleviates hepatic steatosis and hypertension in high fructose-fed rats. 骆驼奶蛋白水解物可缓解高果糖喂养大鼠的肝脏脂肪变性和高血压。
IF 3.9 3区 医学
Pharmaceutical Biology Pub Date : 2022-12-01 DOI: 10.1080/13880209.2022.2079678
Mohammad A Alshuniaber, Ghedeir M Alshammari, Samy M Eleawa, Abu ElGasim A Yagoub, Abdullrahman S Al-Khalifah, Maha H Alhussain, Laila Naif Al-Harbi, Mohammed Abdo Yahya
{"title":"Camel milk protein hydrosylate alleviates hepatic steatosis and hypertension in high fructose-fed rats.","authors":"Mohammad A Alshuniaber, Ghedeir M Alshammari, Samy M Eleawa, Abu ElGasim A Yagoub, Abdullrahman S Al-Khalifah, Maha H Alhussain, Laila Naif Al-Harbi, Mohammed Abdo Yahya","doi":"10.1080/13880209.2022.2079678","DOIUrl":"10.1080/13880209.2022.2079678","url":null,"abstract":"<p><strong>Context: </strong>Camel milk is used in traditional medicine to treat diabetes mellitus hypertension and other metabolic disorders.</p><p><strong>Objective: </strong>This study evaluated the antisteatotic and antihypertensive effects of camel milk protein hydrolysate (CMH) in high fructose (HF)-fed rats and compared it with the effects afforded by the intact camel milk protein extract (ICM).</p><p><strong>Materials and methods: </strong>Adult male Wistar rats were divided into 6 groups (<i>n</i> = 8 each) as 1) control, 2) ICM (1000 mg/kg), 3) CMH (1000 mg/kg), 4) HF (15% in drinking water), 5) HF (15%) + ICM (1000 mg/kg), and 6) HF (15%) + CMH (1000 mg/kg). All treatments were given orally for 21 weeks, daily.</p><p><strong>Results: </strong>Both ICM and CMH reduced fasting glucose and insulin levels, serum and hepatic levels of cholesterol and triglycerides, and serum levels of ALT and AST, angiotensin II, ACE, endothelin-1, and uric acid in HF-fed rats. In addition, both ICM and CMH reduced hepatic fat deposition in the hepatocytes and reduced hepatocyte damage. This was associated with an increase in the hepatic activity of AMPK, higher PPARα mRNA, reduced expression of fructokinase C, SREBP1, SREBP2, fatty acid synthase, and HMG-CoA-reductase. Both treatments lowered systolic and diastolic blood pressure. However, the effects of CMH on all these parameters were greater as compared to ICM.</p><p><strong>Discussion and conclusions: </strong>The findings of this study encourage the use of CMH in a large-scale population and clinical studies to treat metabolic steatosis and hypertension.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"60 1","pages":"1137-1147"},"PeriodicalIF":3.9,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/37/c2/IPHB_60_2079678.PMC9176680.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9073321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The vital role of animal, marine, and microbial natural products against COVID-19. 动物、海洋和微生物天然产物对COVID-19的重要作用
IF 3.9 3区 医学
Pharmaceutical Biology Pub Date : 2022-12-01 DOI: 10.1080/13880209.2022.2039215
Aljawharah A Alqathama, Rizwan Ahmad, Ruba B Alsaedi, Raghad A Alghamdi, Ekram H Abkar, Rola H Alrehaly, Ashraf N Abdalla
{"title":"The vital role of animal, marine, and microbial natural products against COVID-19.","authors":"Aljawharah A Alqathama, Rizwan Ahmad, Ruba B Alsaedi, Raghad A Alghamdi, Ekram H Abkar, Rola H Alrehaly, Ashraf N Abdalla","doi":"10.1080/13880209.2022.2039215","DOIUrl":"10.1080/13880209.2022.2039215","url":null,"abstract":"<p><strong>Context: </strong>Since the outbreak of SARS-CoV-2, researchers have been working on finding ways to prevent viral entry and pathogenesis. Drug development from naturally-sourced pharmacological constituents may be a fruitful approach to COVID-19 therapy.</p><p><strong>Objective: </strong>Most of the published literature has focussed on medicinal plants, while less attention has been given to biodiverse sources such as animal, marine, and microbial products. This review focuses on highlighting natural products and their derivatives that have been evaluated for antiviral, anti-inflammatory, and immunomodulatory properties.</p><p><strong>Methods: </strong>We searched electronic databases such as PubMed, Scopus, Science Direct and Springer Link to gather raw data from publications up to March 2021, using terms such as 'natural products', marine, micro-organism, and animal, COVID-19. We extracted a number of documented clinical trials of products that were tested <i>in silico, in vitro</i>, and <i>in vivo</i> which paid specific attention to chemical profiles and mechanisms of action.</p><p><strong>Results: </strong>Various classes of flavonoids, 2 polyphenols, peptides and tannins were found, which exhibit inhibitory properties against viral and host proteins, including 3CLpro, PLpro, S, hACE2, and NF-κB, many of which are in different phases of clinical trials.</p><p><strong>Discussion and conclusions: </strong>The synergistic effects of logical combinations with different mechanisms of action emphasizes their value in COVID19 management, such as iota carrageenan nasal spray, ermectin oral drops, omega-3 supplementation, and a quadruple treatment of zinc, quercetin, bromelain, and vitamin C. Though <i>in vivo</i> efficacy of these compounds has yet to be established, these bioproducts are potentially useful in counteracting the effects of SARS-CoV-2.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"60 1","pages":"509-524"},"PeriodicalIF":3.9,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8896193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48355901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Curcumin inhibits cerebral ischaemia-reperfusion injury and cell apoptosis in rats through the ERK-CHOP-caspase-11 pathway. 姜黄素通过ERK-CHOP-caspase-11途径抑制大鼠脑缺血再灌注损伤和细胞凋亡。
IF 3.8 3区 医学
Pharmaceutical Biology Pub Date : 2022-12-01 DOI: 10.1080/13880209.2022.2069271
Yue Chen, Lixia Zhang, Zengtai Yang, Jie Yu
{"title":"Curcumin inhibits cerebral ischaemia-reperfusion injury and cell apoptosis in rats through the ERK-CHOP-caspase-11 pathway.","authors":"Yue Chen,&nbsp;Lixia Zhang,&nbsp;Zengtai Yang,&nbsp;Jie Yu","doi":"10.1080/13880209.2022.2069271","DOIUrl":"https://doi.org/10.1080/13880209.2022.2069271","url":null,"abstract":"<p><strong>Context: </strong>Curcumin has a significant effect on cerebral ischaemia-reperfusion injury (CIRI). However, the underlying mechanism is less studied.</p><p><strong>Objective: </strong>This study investigates the role and mechanism of curcumin in CIRI.</p><p><strong>Materials and methods: </strong>CIRI model Sprague-Dawley rats were divided into model, positive control and curcumin low/middle/high dose (50, 100 and 200 mg/kg/d) groups (<i>n</i> = 10 each). Drug intervention was administered by gavage once a day for 4 weeks. We calculated the neurobehavioural score and observed the cerebral infarct volume. Glial cytopathological changes were observed after haematoxylin-eosin staining. Apoptosis was detected by TUNEL (TdT mediated dUTP nick end labelling). Extracellular signal-regulated protein kinase (<i>ERK</i>), C/EBP-homologous protein (<i>CHOP</i>) and <i>caspase-11</i> mRNA were detected by real-time PCR. Phosphorylated ERK (p-ERK), phosphorylated CHOP (p-CHOP) and caspase-11 were detected by Western blot. Superoxide dismutase (SOD) activity was detected by xanthine oxidation method; malondialdehyde (MDA) content by thiobarbituric acid colorimetry; and, glutathione (GSH) by spectrophotometry.</p><p><strong>Results: </strong>Compared with control, the neurobehavioural scores, neuronal apoptosis, MDA, IL-1β, IL-18, mRNAs and protein levels of ERK/p-ERK, CHOP/p-CHOP and caspase-11 in model group were significantly higher (<i>p</i> < 0.01). Compared with model, the positive control and medium/high dose curcumin groups were significantly lower (<i>p</i> < 0.01). However, SOD and GSH decreased significantly in model group but increased significantly in positive control and medium/high dose curcumin groups (<i>p</i> < 0.01). Moreover, curcumin significantly alleviated ischaemic state and neuroinflammation (<i>p</i> < 0.01).</p><p><strong>Discussion and conclusions: </strong>Curcumin may alleviate CIRI through ERK-CHOP-caspase-11 pathway. Our results may provide new insights into the pathogenesis of CIRI, and contribute to the development of treatment strategies for CIRI.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"60 1","pages":"854-861"},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9132463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10566822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Ellagic acid protects against non-alcoholic fatty liver disease in streptozotocin-diabetic rats by activating AMPK. 鞣花酸通过激活AMPK来预防链脲佐菌素糖尿病大鼠的非酒精性脂肪性肝病。
IF 3.8 3区 医学
Pharmaceutical Biology Pub Date : 2022-12-01 DOI: 10.1080/13880209.2021.1990969
Jozaa Z ALTamimi, Ghedeir M Alshammari, Nora A AlFaris, Reham I Alagal, Dalal H Aljabryn, Norah A Albekairi, Mahmoud Ahmad Alkhateeb, Mohammed Abdo Yahya
{"title":"Ellagic acid protects against non-alcoholic fatty liver disease in streptozotocin-diabetic rats by activating AMPK.","authors":"Jozaa Z ALTamimi,&nbsp;Ghedeir M Alshammari,&nbsp;Nora A AlFaris,&nbsp;Reham I Alagal,&nbsp;Dalal H Aljabryn,&nbsp;Norah A Albekairi,&nbsp;Mahmoud Ahmad Alkhateeb,&nbsp;Mohammed Abdo Yahya","doi":"10.1080/13880209.2021.1990969","DOIUrl":"https://doi.org/10.1080/13880209.2021.1990969","url":null,"abstract":"<p><strong>Context: </strong>Ellagic acid (EA) is used in traditional medicine to treated hyperlipidaemia.</p><p><strong>Objective: </strong>This study examined if AMPK mediates the anti-steatotic effect of ellagic acid (EA) in streptozotocin (STZ)-induced type 1 diabetes mellitus in rats.</p><p><strong>Materials and methods: </strong>Adult male Wistar rats (130 ± 10 g) were divided into 6 groups (<i>n</i> = 8 rats/group) as control, control + EA, control + EA + CC an AMPK inhibitor), T1DM, T1DM + EA, and T1DM + EA + CC. The treatments with EA (50 mg/kg/orally) and CC (200 ng/rat/i.p.) were given the desired groups for 12 weeks, daily.</p><p><strong>Results: </strong>In T1DM-rats, EA reduced fasting glucose levels (44.8%), increased fasting insulin levels (92.8%), prevented hepatic lipid accumulation, and decreased hepatic and serum levels of total triglycerides (54% & 61%), cholesterol (57% & 48%), and free fatty acids (40% & 37%). It also reduced hepatic levels of ROS (62%), MDA (52%), TNF-α (62%), and IL-6 (57.2%) and the nuclear activity of NF-κB p65 (54%) but increased the nuclear activity of Nrf-2 (4-fold) and levels of GSH (107%) and SOD (87%). Besides, EA reduced downregulated SREBP1 (35%), SREBP2 (34%), ACC-1 (36%), FAS (38%), and HMG-CoAR (49%) but stimulated mRNA levels of PPARα (1.7-fold) and CPT1a (1.8-fold), CPT1b (2.9-fold), and p-AMPK (4-fold). All these events were prevented by the co-administration of CC.</p><p><strong>Discussion and conclusions: </strong>These findings encourage the use of EA to treat hepatic disorders, and non-alcoholic fatty liver disease (NAFLD). Further <i>in vivo</i> and <i>in vitro</i> studies are needed to validate its potential in clinical medicine.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"60 1","pages":"25-37"},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8654409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9072793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 20
A tribute to Prof. em. Dr. Dr. h.c. mult. Hildebert Wagner. 致敬m教授。h。c。mult博士。Hildebert瓦格纳。
IF 3.8 3区 医学
Pharmaceutical Biology Pub Date : 2022-12-01 DOI: 10.1080/13880209.2022.2045067
Rudolf Bauer
{"title":"A tribute to Prof. em. Dr. Dr. h.c. mult. Hildebert Wagner.","authors":"Rudolf Bauer","doi":"10.1080/13880209.2022.2045067","DOIUrl":"https://doi.org/10.1080/13880209.2022.2045067","url":null,"abstract":"","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"60 1","pages":"i-iii"},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8920382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9417172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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