Pub Date : 2016-01-01Epub Date: 2016-06-20DOI: 10.4172/2167-0501.1000213
Lin L, Wang X, Yu Z
Ischemia-reperfusion injury is a common feature of ischemic stroke, which occurs when blood supply is restored after a period of ischemia. Reperfusion can be achieved either by thrombolysis using thrombolytic reagents such as tissue plasminogen activator (tPA), or through mechanical removal of thrombi. Spontaneous reperfusion also occurs after ischemic stroke. However, despite the beneficial effect of restored oxygen supply by reperfusion, it also causes deleterious effect compared with permanent ischemia. With the recent advancement in endovascular therapy including thrombectomy and thrombus disruption, reperfusion-injury has become an increasingly critical challenge in stroke treatment. It is therefore of extreme importance to understand the mechanisms of ischemia-reperfusion injury in the brain in order to develop effective therapeutics. Accumulating experimental evidence have suggested that the mechanisms of ischemia-reperfusion injury include oxidative stress, leukocyte infiltration, platelet adhesion and aggregation, complement activation, mitochondrial mediated mechanisms, and blood-brain-barrier (BBB) disruption, which altogether ultimately lead to edema or hemorrhagic transformation (HT) in the brain. Potential therapeutic strategies against ischemia-reperfusion injury may be developed targeting these mechanisms. In this review, we briefly discuss the pathophysiology and cellular and molecular mechanisms of cerebral ischemia-reperfusion injury, and potential therapeutic strategies.
{"title":"Ischemia-reperfusion Injury in the Brain: Mechanisms and Potential Therapeutic Strategies.","authors":"Lin L, Wang X, Yu Z","doi":"10.4172/2167-0501.1000213","DOIUrl":"https://doi.org/10.4172/2167-0501.1000213","url":null,"abstract":"<p><p>Ischemia-reperfusion injury is a common feature of ischemic stroke, which occurs when blood supply is restored after a period of ischemia. Reperfusion can be achieved either by thrombolysis using thrombolytic reagents such as tissue plasminogen activator (tPA), or through mechanical removal of thrombi. Spontaneous reperfusion also occurs after ischemic stroke. However, despite the beneficial effect of restored oxygen supply by reperfusion, it also causes deleterious effect compared with permanent ischemia. With the recent advancement in endovascular therapy including thrombectomy and thrombus disruption, reperfusion-injury has become an increasingly critical challenge in stroke treatment. It is therefore of extreme importance to understand the mechanisms of ischemia-reperfusion injury in the brain in order to develop effective therapeutics. Accumulating experimental evidence have suggested that the mechanisms of ischemia-reperfusion injury include oxidative stress, leukocyte infiltration, platelet adhesion and aggregation, complement activation, mitochondrial mediated mechanisms, and blood-brain-barrier (BBB) disruption, which altogether ultimately lead to edema or hemorrhagic transformation (HT) in the brain. Potential therapeutic strategies against ischemia-reperfusion injury may be developed targeting these mechanisms. In this review, we briefly discuss the pathophysiology and cellular and molecular mechanisms of cerebral ischemia-reperfusion injury, and potential therapeutic strategies.</p>","PeriodicalId":8764,"journal":{"name":"Biochemistry & Pharmacology: Open Access","volume":"5 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2167-0501.1000213","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36210319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2015-12-01DOI: 10.4172/2167-0501.1000199
TP Shareena Dasari, Y. Zhang, H. Yu
Gold nanoparticles (AuNPs) and gold ion complexes have been investigated for their antibacterial activities. However, the majority of the reports failed to disclose the concentration of free Au(I) or Au(III) present in solutions of AuNPs or gold ion complexes. The inconsistency of antibacterial activity of AuNPs may be due to the effect of the presence of Au(III). Here we report the antibacterial activity of Au(I) and Au(III) to four different bacteria: one nonpathogenic bacterium: E. coli and three multidrug-resistant bacteria: E. coli, S. typhimurium DT104, and S. aureus. Au(I) and Au(III) as chloride are highly toxic to all the four bacteria, with IC50 of 0.35 – 0.49 µM for Au(III) and 0.27–0.52 µM for Au(I).The bacterial growth inhibition by both Au(I) and Au(III) increases with exposure time and is strongly affected by the use of buffers. The IC50 values for Au(I) and Au(III) in different buffers are HEPES (0.48 and 1.55 µM) > Trizma (0.41 and 0.57 µM) > PBS (0.14 and 0.06 µM). Bacterial growth inhibition by AuNPs is gradually reduced by centrifugation-resuspension to remove residual Au(III) ion present in the crude synthetic AuNPs. After 4 centrifugations-resuspensions, AuNPs become non-toxic. In addition, both Au(I) and Au(III) are cytotoxic to skin keratinocyte and blood lymphocyte cells. These results suggest that Au(I) and Au(III) in pure or complex forms may be explored as a method to treat drug-resistant bacteria, and the test of AuNPs toxicity must consider residual Au(III), exposure time, and the use of buffers.
{"title":"Antibacterial Activity and Cytotoxicity of Gold (I) and (III) Ions and Gold Nanoparticles","authors":"TP Shareena Dasari, Y. Zhang, H. Yu","doi":"10.4172/2167-0501.1000199","DOIUrl":"https://doi.org/10.4172/2167-0501.1000199","url":null,"abstract":"Gold nanoparticles (AuNPs) and gold ion complexes have been investigated for their antibacterial activities. However, the majority of the reports failed to disclose the concentration of free Au(I) or Au(III) present in solutions of AuNPs or gold ion complexes. The inconsistency of antibacterial activity of AuNPs may be due to the effect of the presence of Au(III). Here we report the antibacterial activity of Au(I) and Au(III) to four different bacteria: one nonpathogenic bacterium: E. coli and three multidrug-resistant bacteria: E. coli, S. typhimurium DT104, and S. aureus. Au(I) and Au(III) as chloride are highly toxic to all the four bacteria, with IC50 of 0.35 – 0.49 µM for Au(III) and 0.27–0.52 µM for Au(I).The bacterial growth inhibition by both Au(I) and Au(III) increases with exposure time and is strongly affected by the use of buffers. The IC50 values for Au(I) and Au(III) in different buffers are HEPES (0.48 and 1.55 µM) > Trizma (0.41 and 0.57 µM) > PBS (0.14 and 0.06 µM). Bacterial growth inhibition by AuNPs is gradually reduced by centrifugation-resuspension to remove residual Au(III) ion present in the crude synthetic AuNPs. After 4 centrifugations-resuspensions, AuNPs become non-toxic. In addition, both Au(I) and Au(III) are cytotoxic to skin keratinocyte and blood lymphocyte cells. These results suggest that Au(I) and Au(III) in pure or complex forms may be explored as a method to treat drug-resistant bacteria, and the test of AuNPs toxicity must consider residual Au(III), exposure time, and the use of buffers.","PeriodicalId":8764,"journal":{"name":"Biochemistry & Pharmacology: Open Access","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75878035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2015-10-01DOI: 10.4172/2167-0501.1000e179
Erick O. Hernández-Ochoa, Camilo Vanegas
Humans build muscle mass over the first two decades of life; begin to lose muscle mass and strength between the third and fourth decades, and the decline accelerates during the sixth decade. Sarcopenia and dynapenia are age-related loss of skeletal muscle mass and muscle strength, respectively.
{"title":"Diabetic Myopathy and Mechanisms of Disease","authors":"Erick O. Hernández-Ochoa, Camilo Vanegas","doi":"10.4172/2167-0501.1000e179","DOIUrl":"https://doi.org/10.4172/2167-0501.1000e179","url":null,"abstract":"Humans build muscle mass over the first two decades of life; begin to lose muscle mass and strength between the third and fourth decades, and the decline accelerates during the sixth decade. Sarcopenia and dynapenia are age-related loss of skeletal muscle mass and muscle strength, respectively.","PeriodicalId":8764,"journal":{"name":"Biochemistry & Pharmacology: Open Access","volume":"33 2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81164395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-01Epub Date: 2014-03-14DOI: 10.4172/2167-0501.1000e157
Sibaprasad Bhattacharyya
{"title":"Progress in Making Ras as a Druggable Target.","authors":"Sibaprasad Bhattacharyya","doi":"10.4172/2167-0501.1000e157","DOIUrl":"10.4172/2167-0501.1000e157","url":null,"abstract":"","PeriodicalId":8764,"journal":{"name":"Biochemistry & Pharmacology: Open Access","volume":"3 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4610733/pdf/nihms655690.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34109145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-03-08DOI: 10.4172/2167-0501.1000131
Joann B Powell, Maryam Ghotbaddini
Polyaromatic hydrocarbons, heterocyclic aromatic amines and dioxin-like compounds are environmental carcinogens shown to initiate cancer in a number of tissue types including prostate and breast. These environmental carcinogens elicit their effects through interacting with the aryl hydrocarbon receptor (AhR), a ligand activated transcription factor. Naturally occurring compounds found in fruits and vegetables shown to have anti-carcinogenic effects also interact with the AhR. This review explores dietary and environmental exposure to chemical carcinogens and beneficial natural compounds whose effects are elicited by the AhR.
{"title":"Cancer-promoting and Inhibiting Effects of Dietary Compounds: Role of the Aryl Hydrocarbon Receptor (AhR).","authors":"Joann B Powell, Maryam Ghotbaddini","doi":"10.4172/2167-0501.1000131","DOIUrl":"https://doi.org/10.4172/2167-0501.1000131","url":null,"abstract":"<p><p>Polyaromatic hydrocarbons, heterocyclic aromatic amines and dioxin-like compounds are environmental carcinogens shown to initiate cancer in a number of tissue types including prostate and breast. These environmental carcinogens elicit their effects through interacting with the aryl hydrocarbon receptor (AhR), a ligand activated transcription factor. Naturally occurring compounds found in fruits and vegetables shown to have anti-carcinogenic effects also interact with the AhR. This review explores dietary and environmental exposure to chemical carcinogens and beneficial natural compounds whose effects are elicited by the AhR.</p>","PeriodicalId":8764,"journal":{"name":"Biochemistry & Pharmacology: Open Access","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2167-0501.1000131","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32699227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-09-24DOI: 10.4172/2167-0501.1000120
Vineet Gupta, Yong-Yu Liu
Diverging from eliminating tumors, many anticancer agents can result in drug resistance and myelosuppression or bone marrow suppression in patients during the course of chemotherapy. Drug resistance and myelosuppression are two major impediments to the success of chemotherapy. Recent study of Bhinge et al. demonstrates that glucosylceramide synthase (GCS) can determine the opposite effects of doxorubicin on breast cancer stem cells versus bone marrow stem cells in vivo [1,2]. These observations disclose new insights on GCS in stem cells that are basis of drug resistance and myelosuppression.
{"title":"New Insights on Glucosylceramide Synthase in Cancer Drug Resistance and Myelosuppression.","authors":"Vineet Gupta, Yong-Yu Liu","doi":"10.4172/2167-0501.1000120","DOIUrl":"https://doi.org/10.4172/2167-0501.1000120","url":null,"abstract":"Diverging from eliminating tumors, many anticancer agents can result in drug resistance and myelosuppression or bone marrow suppression in patients during the course of chemotherapy. Drug resistance and myelosuppression are two major impediments to the success of chemotherapy. Recent study of Bhinge et al. demonstrates that glucosylceramide synthase (GCS) can determine the opposite effects of doxorubicin on breast cancer stem cells versus bone marrow stem cells in vivo [1,2]. These observations disclose new insights on GCS in stem cells that are basis of drug resistance and myelosuppression.","PeriodicalId":8764,"journal":{"name":"Biochemistry & Pharmacology: Open Access","volume":"2 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2167-0501.1000120","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32817906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2012-08-08DOI: 10.4172/2167-0501.1000e128
Sibaprasad Bhattacharyya
Positron Emission Tomography (PET) is a clinically established noninvasive imaging modality. In PET, targeting ligands, or drug molecules labeled with a positron-emitting isotope, typically known as PET-radiopharmaceuticals, are introduced in to the body at a very low concentration (nanomolar or picomolar range), and are not intended to have any pharmacological effect.
{"title":"Application of Positron Emission Tomography in Drug Development.","authors":"Sibaprasad Bhattacharyya","doi":"10.4172/2167-0501.1000e128","DOIUrl":"https://doi.org/10.4172/2167-0501.1000e128","url":null,"abstract":"Positron Emission Tomography (PET) is a clinically established noninvasive imaging modality. In PET, targeting ligands, or drug molecules labeled with a positron-emitting isotope, typically known as PET-radiopharmaceuticals, are introduced in to the body at a very low concentration (nanomolar or picomolar range), and are not intended to have any pharmacological effect.","PeriodicalId":8764,"journal":{"name":"Biochemistry & Pharmacology: Open Access","volume":"1 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2012-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2167-0501.1000e128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32772928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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