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Strengthening pharmacotherapy research for COVID-19-induced pulmonary fibrosis

World Journal of Clinical Cases 2024年第5期12卷 875-879页

作者： Yan-Miao Liu Jing Zhang Jing-Jing Wu Wei-Wei Guo Fu-Shan Tang The First Clinical Institute Zunyi Medical UniversityZunyi 563006Guizhou ProvinceChina Key laboratory of Clinical Pharmacy in Zunyi City Zunyi Medical UniversityZunyi 563006Guizhou ProvinceChina Department of Respiratory Medicine Central Hospital in Jinchang CityJinchang 737102Gansu ProvinceChina Department of Clinical Pharmacy Key Laboratory of Basic Pharmacology of Guizhou Province and School of PharmacyZunyi Medical UniversityZunyi 563006Guizhou ProvinceChina Key laboratory of Basic Pharmacology of Ministry of Education and Joint International Research laboratory of Ethnomedicine of Ministry of Education Zunyi Medical UniversityZunyi 563006Guizhou ProvinceChina

The global spread of severe acute respiratory syndrome coronavirus 2 has resulted in a significant number of individuals developing pulmonary fibrosis(PF),an irreversible lung injury.This condition can manifest within a short inter-val following the onset of pneumonia symptoms,sometimes even within a few days.While lung transplantation is a potentially lifesaving procedure,its limited availability,high costs,intricate surgeries,and risk of immunological rejection present significant drawbacks.The optimal timing of medication administration for coronavirus disease 2019(COVID-19)-induced PF remains controversial.Despite this,it is crucial to explore pharmacotherapy interventions,involving early and preventative treatment as well as pharmacotherapy options for advanced-stage PF.Additionally,studies have demonstrated disparities in anti-fibrotic treatment based on race and gender factors.Genetic mutations may also impact therapeutic efficacy.Enhancing research efforts on pharmacotherapy interventions,while considering relevant pharmacological factors and optimizing the timing and dosage of medication administration,will lead to enhanced,personalized,and fair treatment for individuals impacted by COVID-19-related PF.These measures are crucial in lessening the burden of the disease on healthcare systems and improving patients'quality of life.

关键词： COVID-19 Pulmonary fibrosis pharmacotherapy intervention Medication administration Timing Dosage

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Glutaredoxin-1 alleviates acetaminophen-induced liver injury by decreasing its toxic metabolites

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Journal of Pharmaceutical Analysis 2023年第12期13卷 1548-1561页

作者： Ying Xu Yan Xia Qinhui Liu Xiandan Jing Qin Tang Jinhang Zhang Qingyi Jia Zijing Zhang Jiahui Li Jiahao Chen Yimin Xiong Yanping Li Jinhan He Department of Pharmacy Institute of Metabolic Diseases and PharmacotherapyWest China HospitalSichuan UniversityChengdu610041China

Excessive N-acetyl-p-benzoquinone imine(NAPQI)formation is a starting event that triggers oxidative stress and subsequent hepatocyte necrosis in acetaminophen(APAP)overdose caused acute liver failure(ALF).S-glutathionylation is a reversible redox post-translational modification and a prospective mechanism of APAP hepatotoxicity.Glutaredoxin-1(Glrx1),a glutathione-specific thioltransferase,is a primary enzyme to catalyze deglutathionylation.The objective of this study was to explored whether and how Glrx1 is associated with the development of ALF induced by APAP.The Glrx1 knockout mice(Glrx1^(-/-))and liver-specific overexpression of Glrx1(AAV8-Glrx1)mice were produced and underwent APAPinduced ALF.Pirfenidone(PFD),a potential inducer of Glrx1,was administrated preceding APAP to assess its protective effects.Our results revealed that the hepatic total protein S-glutathionylation(PSSG)increased and the Glrx1 level reduced in mice after APAP toxicity.Glrx1^(-/-)mice were more sensitive to APAP overdose,with higher oxidative stress and more toxic metabolites of APAP.This was attributed to Glrx1 deficiency increasing the total hepatic PSSG and the S-glutathionylation of cytochrome p4503a11(Cyp3a11),which likely increased the activity of Cyp3a11.Conversely,AAV8-Glrx1 mice were defended against liver damage caused by APAP overdose by inhibiting the S-glutathionylation and activity of Cyp3a11,which reduced the toxic metabolites of APAP and oxidative stress.PFD precede administration upregulated Glrx1 expression and alleviated APAP-induced ALF by decreasing oxidative stress.We have identified the function of Glrx1 mediated PSSG in liver injury caused by APAP overdose.Increasing Glrx1 expression may be investigated for the medical treatment of APAP-caused hepatic injury.

关键词： Glutaredoxin-1 S-glutathionylation Acetaminophen Toxic metabolites Cyp3a11

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Effects of tomato juice on the pharmacokinetics of CYP3A4-substrate drugs

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Asian Journal of Pharmaceutical Sciences 2017年第5期12卷 464-469页

作者： Atsuko Ohkubo Tomomi Chida Hidetomo Kikuchi Tadashi Tsuda Katsuyoshi Sunaga laboratory of pharmacotherapy Department of Clinical Dietetics and Human Nutrition Faculty of Pharmaceutical Sciences Josai University

We previously demonstrated that tomato juice(TJ) contains potent mechanism-based inhibitor(s) of CYP3A4. In this study, we investigated the effects of TJ and grapefruit juice(GFJ)on the pharmacokinetics of the CYP3A4-substrate drugs, nifedipine(NFP) and midazolam(MDZ), in male Wistar rats. Oral administration of GFJ 90 min before the intraduodenal administration of NFP or MDZ increased the area under the concentration–time curves(AUCs)of NFP and MDZ by 32.4% and 89.4%, respectively. TJ increased MDZ blood concentrations and AUC after intraduodenal MDZ administration;however, it had no effect on NFP. When MDZ and NFP were intravenously administered, GFJ significantly increased the AUC of MDZ,but only slightly increased that of NFP. In contrast, TJ only slightly increased the AUC of MDZ.These results suggest that, similar to GFJ, TJ influences the pharmacokinetics of CYP3A4-substrate drugs;however, it may be a drug-dependent partial effect.

关键词： Food–drug interactions Tomato juice Grapefruit juice Nifedipine Midazolam Pharmacokinetic interactions

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Induction of Sirtuin1 Activity in SH-SY5Y Cells by Cyanidin-3-O-Glucocide Induced

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Pharmacology & Pharmacy 2022年第2期13卷 35-48页

作者： Kaori Yama Yoshiki Hasebe Ayuka Inomata Jun Miura Ainari Konda pharmacotherapy Hokkaido University of Science Sapporo Japan

An increase in oxidative stress plays a key role in neurotoxicity induction and cell death, which leads to neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease. Cyanidin-3-glucoside (C3G) is a common anthocyanin and shows antioxidant activity in neuronal cells. Silent information regulator 2-related protein 1 (Sirt1) regulates antioxidant and anti-inflammatory effects. However, the effects of C3G on Sirt1 in neuronal cells remain unclear. This study evaluated the effect of C3G on Sirt1 expression and activity in human neuroblastoma (SH-SY5Y) cells. In the study, C3G increased the expression of Sirt1 and Sirt1 activity in SH-SY5Y cells. Additionally, C3G increased the expression of nuclear factor erythroid 2-related factor 2, a vital transcription factor for regulating the expression of antioxidant genes, as well as antioxidant enzymes such as superoxide dismutase and catalase. Moreover, C3G protected SH-SY5Y cells from oxidative stress. These results suggest that C3G decreased oxidative stress-induced cell injury by increasing the expression of Sirt1 and other antioxidant factors. Therefore, C3G might merit further investigation for use in attenuating the progress of neurodegenerative diseases.

关键词： Cyanidin-3-O-Glucocide Sirtuin1 Anti-Senescence Antioxidant Oxidative Stress Nerve Cells

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Preliminary in vitro evaluation of neuroprotective and monoamine oxidase type B inhibitory effects of newly synthesized 8-aminocaffeines

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Neural Regeneration Research 2019年第6期14卷 971-972页

作者： Magdalena Kondeva-Burdina Maya Georgieva Alexandra Kasabova-Angelova Virginia Tzankova Alexander Zlatkov laboratory of Drug Metabolism and Drug Toxicity Department of PharmacologyPharmacotherapy and ToxicologyFaculty of PharmacyMedical University of Sofia Department of Pharmaceutical Chemistry Faculty of PharmacyMedical University of Sofia

The expected growth of the elderly population at highest risk for Parkinson’s disease(PD)in the next decades makes the identification of factors that promote or prevent the disease an important goal.In addition,new therapies-aiming to delay the progression of PD are also needed(Prediger,2010).However,there have been few clinical trials designed to investigate neuroprotection.Thus the application of an appropriate in vitro model such as the neuroblastoma SH-SY5Y cell line is extremely helpful.These cells were selected due to its human origin,catecholaminergic neuronal properties,and ease of maintenance(Xicoy et al.,2017).

关键词： Preliminary neuroprotective monoamine oxidase

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The cGAS-STING signaling in cardiovascular and metabolic diseases: Future novel target option for pharmacotherapy

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Acta Pharmaceutica Sinica B 2022年第1期12卷 50-75页

作者： Patrick Kwabena Oduro Xianxian Zheng Jinna Wei Yanze Yang Yuefei Wang Han Zhang Erwei Liu Xiumei Gao Mei Du Qilong Wang Institute of Traditional Chinese Medicine Tianjin University of Traditional Chinese MedicineTianjin 301617China State Key laboratory of Component-Based Chinese Medicine Ministry of EducationTianjin 301617China Department of Pharmacology and Tianjin Key laboratory of Inflammation Biology School of Basic Medical SciencesTianjin Medical UniversityTianjin 300070China

The cyclic GMP-AMP synthase(cGAS)-stimulator of interferon genes(STING) signaling exert essential regulatory function in microbial-and onco-immunology through the induction of cytokines, primarily type I interferons. Recently, the aberrant and deranged signaling of the cGAS-STING axis is closely implicated in multiple sterile inflammatory diseases, including heart failure,myocardial infarction, cardiac hypertrophy, nonalcoholic fatty liver diseases, aortic aneurysm and dissection, obesity, etc. This is because of the massive loads of damage-associated molecular patterns(mitochondrial DNA, DNA in extracellular vesicles) liberated from recurrent injury to metabolic cellular organelles and tissues, which are sensed by the pathway. Also, the cGAS-STING pathway crosstalk with essential intracellular homeostasis processes like apoptosis, autophagy, and regulate cellular metabolism.Targeting derailed STING signaling has become necessary for chronic inflammatory diseases. Meanwhile, excessive type I interferons signaling impact on cardiovascular and metabolic health remain entirely elusive. In this review, we summarize the intimate connection between the cGAS-STING pathway and cardiovascular and metabolic disorders. We also discuss some potential small molecule inhibitors for the pathway. This review provides insight to stimulate interest in and support future research into understanding this signaling axis in cardiovascular and metabolic tissues and diseases.

关键词： STING cGAS Cardiovascular diseases Metabolic diseases Damage-associated molecular patterns Inflammation ER stress Mitochondria

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Identification of anthelmintic parbendazole as a therapeutic molecule for HNSCC through connectivity map-based drug repositioning

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Acta Pharmaceutica Sinica B 2022年第5期12卷 2429-2442页

作者： Dong Liang Chen Yu Zhao Ma Xingye Yang Zhenzhen Li Xuhui Dong Xiaojun Qin Lupei Du Minyong Li Key laboratory of Chemical Biology(MOE) School of Pharmaceutical SciencesCheeloo College of MedicineShandong UniversityJinan 250012China

Head and neck squamous cell carcinoma(HNSCC) is one of the most common human cancers;however, its outcome of pharmacotherapy is always very limited. Herein, we performed a batch query in the connectivity map(cMap) based on bioinformatics, queried out 35 compounds with therapeutic potential, and screened out parbendazole as a most promising compound, which had an excellent inhibitory effect on the proliferation of HNSCC cell lines. In addition, tubulin was identified as a primary target of parbendazole, and the direct binding between them was further verified. Parbendazole was further proved as an effective tubulin polymerization inhibitor, which can block the cell cycle, cause apoptosis and prevent cell migration, and it exhibited reasonable therapeutic effect and low toxicity in the in vivo and in vitro anti-tumor evaluation. Our study repositioned an anthelmintic parbendazole to treat HNSCC, which revealed a therapeutic utility and provided a new treatment option for human cancers.

关键词： HNSCC cMap Bioinformatics Parbendazole Drug repositioning Anti-tumor

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Deterioration of Dry Skin in Arthritis Model Mice via Stress-Induced Changes in Immune Cells in the Thymus and Spleen

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Journal of Biosciences and Medicines 2020年第1期8卷 23-37页

作者： Kenji Goto Keiichi Hiramoto Ion Takada Kazuya Ooi laboratory of Clinical Pharmacology Faculty of Pharmaceutical Sciences Suzuka University of Medical Science Suzuka Japan laboratory of Pathophysiology and pharmacotherapy Faculty of Pharmaceutical Sciences Suzuka University of Medical Science Suzuka Japan

Objective: Skin dryness is a characteristic of rheumatoid arthritis model mice. A previous study reported that the stress hormone glucocorticoid (i.e., corticosterone) is related to the induction of dry skin in arthritic mice. However, the mechanism through which stress induces dry skin in these mice is still unclear. Therefore, in this study, we examined the relationship between stress and induction of dry skin in arthritic mice. Methods: Physical stress load in mice with DBA/1JJmsSlc collagen-induced arthritis was treated with water immersion stress, and transepidermal water loss and the expression of markers associated with allergic reactions and inflammation was evaluated. Results: Deterioration of skin dryness was observed in stressed arthritic mice compared with that in unstressed arthritic mice. Moreover, plasma levels of interleukin-6 and corticosterone were increased in stressed arthritic mice compared with those in unstressed arthritic mice. We also observed decreased regulatory T cell numbers and increased T helper type 2 cell numbers in the thymus of stressed arthritic mice compared with those in unstressed arthritic mice. Conclusion: These results suggested that abnormalities in the immune system were related to deterioration of dry skin in stressed arthritic mice. Thus, reduction of stress may prevent deterioration of dry skin in mice with arthritis.

关键词： Arthritis Dry Skin Stress Helper T Cells Regulatory T Cells

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Hepatic Antifibrotic pharmacotherapy:Are We Approaching Success?

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Journal of Clinical and Translational Hepatology 2020年第2期8卷 222-229页

作者： Yue Chang Hai Li Division of Gastroenterology and Hepatology Tianjin Xiqing HospitalTianjinChina Tianjin Key laboratory of Hepatopancreatic Fibrosis and Molecular Diagnosis and Treatment TianjinChina

The incidence rate and mortality of liver fibrosis caused by various etiologies are high throughout the world. Liver fibrosis, the subsequent cirrhosis and other serious related complications threaten the health of patients and represent a serious medical burden;yet, there is still a lack of approved methods to prevent or reverse liver fibrosis. Therefore, effective hepatic antifibrotic drugs are urgently needed. The activation and proliferation of hepatic stellate cells are still the mechanisms of fibrosis that remain the focus of therapeutic research. In recent years, significant progress has been made in the development and applicability of antifibrosis drugs. In this review, we summarize the effectiveness and safety of available antifibrosis drugs utilizing different targets. In addition, some characteristics of antifibrosis drugs in phase II and III trials are introduced in detail.

关键词： Antifibrotic agents Fibrosis Liver Reversal pharmacotherapy

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The fate of medications evaluated for ischemic stroke pharmacotherapy over the period 1995–2015

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Acta Pharmaceutica Sinica B 2016年第6期6卷 522-530页

作者： Xiaoling Chen Kewei Wang Department of Molecular and Cellular Pharmacology State Key Laboratory of Natural and Biomimetic Drugs Peking University School of Pharmaceutical Sciences Department of Pharmacology Qingdao University School of Pharmacy

Stroke is a brain damage caused by a loss of blood supply to a portion of the brain, which requires prompt and effective treatment. The current pharmacotherapy for ischemic stroke primarily relies on thrombolysis using recombinant tissue plasminogen activators(rt-PAs) to breakdown blood clots. Neuroprotective agents that inhibit excitatory neurotransmitters are also used to treat ischemic stroke but have failed to translate into clinical benefits. This poses a major challenge in biomedical research to understand what causes the progressive brain cell death after stroke and how to develop an effective pharmacotherapy for stroke. This brief review analyzes the fate of about 430 potentially useful stroke medications over the period 1995–2015and describes in detail those that successfully reached the market. Hopefully, the information from this analysis will shed light on how future stroke research can improve stroke drug discovery.

关键词： Thrombosis Neuroprotective agent Ischemic stroke Traditional Chinese medicine Non-NMDA mechanism Ion channel

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