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  1. Article ; Online: Use of bee venom in preventive medicine

    Mustafa Bayraktar / Ahmet Hacımüftüoğlu / Ufuk Okkay / Mehmet Nuri Koçak / Murat Kösedağ / Erdal Tekin / Muhammet Çelik / Irmak Ferah Okkay / Cemil Bayram / Muhammet Sait Ertuğrul / Selma Sezen

    Veterinary Medicine and Science, Vol 10, Iss 1, Pp n/a-n/a (2024)

    An experimental hepatic encephalopathy study in rats

    2024  

    Abstract: Abstract Objectives Bee venom is used for medicinal purposes, including the treatment of neurological and liver diseases, but its use as a primary health care approach for preventive purposes requires further exploration. The aim of this study was to ... ...

    Abstract Abstract Objectives Bee venom is used for medicinal purposes, including the treatment of neurological and liver diseases, but its use as a primary health care approach for preventive purposes requires further exploration. The aim of this study was to provide the first investigation into the possible protective effects of bee venom against hepatic encephalopathy, a serious neurodegenerative disease. Materials and Methods An experimental animal study was conducted in which healthy albino Sprague–Dawley rats were randomized into three groups: healthy, control and bee venom groups. All rats were tested for locomotor activity at the beginning and end of the study. No intervention was made in the healthy group, whereas hepatic encephalopathy was induced in the control and bee venom groups by the administration of thioacetamide (TAA) (200 mg/kg/day). The bee venom group also received bee venom (5 mg/kg/day) subcutaneously every day for 14 days prior to the TAA administration. Results The results for the final locomotor activity tests were statistically better in the bee venom group than in the control group, supporting a beneficial effect of prophylactic bee venom application. Blood ammonia levels and liver weights, determined as indicators of inflammation, were lower in the bee venom group than in the control group and were close to levels in the healthy group, but not statistically significant. Conclusions Bee venom administration has protective effects against the development of hepatic encephalopathy and offers a promising therapeutic opportunity in preventive medicine.
    Keywords Bee venom ; hepatic encephalopathy ; prevention ; primary care ; Veterinary medicine ; SF600-1100
    Subject code 630
    Language English
    Publishing date 2024-01-01T00:00:00Z
    Publisher Wiley
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Discovery of therapeutic agents targeting PKLR for NAFLD using drug repositioning

    Cheng Zhang / Mengnan Shi / Woonghee Kim / Muhammad Arif / Martina Klevstig / Xiangyu Li / Hong Yang / Cemil Bayram / Ismail Bolat / Özlem Özdemir Tozlu / Ahmet Hacımuftuoglu / Serkan Yıldırım / Jihad Sebhaoui / Shazia Iqbal / Yongjun Wei / Xiaojing Shi / Jens Nielsen / Hasan Turkez / Mathias Uhlen /
    Jan Boren / Adil Mardinoglu

    EBioMedicine, Vol 83, Iss , Pp 104214- (2022)

    2022  

    Abstract: Summary: Background: Non-alcoholic fatty liver disease (NAFLD) encompasses a wide spectrum of liver pathologies. However, no medical treatment has been approved for the treatment of NAFLD. In our previous study, we found that PKLR could be a potential ... ...

    Abstract Summary: Background: Non-alcoholic fatty liver disease (NAFLD) encompasses a wide spectrum of liver pathologies. However, no medical treatment has been approved for the treatment of NAFLD. In our previous study, we found that PKLR could be a potential target for treatment of NALFD. Here, we investigated the effect of PKLR in in vivo model and performed drug repositioning to identify a drug candidate for treatment of NAFLD. Methods: Tissue samples from liver, muscle, white adipose and heart were obtained from control and PKLR knockout mice fed with chow and high sucrose diets. Lipidomics as well as transcriptomics analyses were conducted using these tissue samples. In addition, a computational drug repositioning analysis was performed and drug candidates were identified. The drug candidates were both tested in in vitro and in vivo models to evaluate their toxicity and efficacy. Findings: The Pklr KO reversed the increased hepatic triglyceride level in mice fed with high sucrose diet and partly recovered the transcriptomic changes in the liver as well as in other three tissues. Both liver and white adipose tissues exhibited dysregulated circadian transcriptomic profiles, and these dysregulations were reversed by hepatic knockout of Pklr. In addition, 10 small molecule drug candidates were identified as potential inhibitor of PKLR using our drug repositioning pipeline, and two of them significantly inhibited both the PKLR expression and triglyceride level in in vitro model. Finally, the two selected small molecule drugs were evaluated in in vivo rat models and we found that these drugs attenuate the hepatic steatosis without side effect on other tissues. Interpretation: In conclusion, our study provided biological insights about the critical role of PKLR in NAFLD progression and proposed a treatment strategy for NAFLD patients, which has been validated in preclinical studies. Funding: ScandiEdge Therapeutics and Knut and Alice Wallenberg Foundation.
    Keywords Systems biology ; Drug repositioning ; NAFLD ; PKLR ; Circadian rhythms ; Medicine ; R ; Medicine (General) ; R5-920
    Subject code 610
    Language English
    Publishing date 2022-09-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Combined metabolic activators improve cognitive functions in Alzheimer’s disease patients

    Burak Yulug / Ozlem Altay / Xiangyu Li / Lutfu Hanoglu / Seyda Cankaya / Simon Lam / Halil Aziz Velioglu / Hong Yang / Ebru Coskun / Ezgi Idil / Rahim Nogaylar / Ahmet Ozsimsek / Cemil Bayram / Ismail Bolat / Sena Oner / Ozlem Ozdemir Tozlu / Mehmet Enes Arslan / Ahmet Hacimuftuoglu / Serkan Yildirim /
    Muhammad Arif / Saeed Shoaie / Cheng Zhang / Jens Nielsen / Hasan Turkez / Jan Borén / Mathias Uhlén / Adil Mardinoglu

    Translational Neurodegeneration, Vol 12, Iss 1, Pp 1-

    a randomised, double-blinded, placebo-controlled phase-II trial

    2023  Volume 23

    Abstract: Abstract Background Alzheimer’s disease (AD) is associated with metabolic abnormalities linked to critical elements of neurodegeneration. We recently administered combined metabolic activators (CMA) to the AD rat model and observed that CMA improves the ... ...

    Abstract Abstract Background Alzheimer’s disease (AD) is associated with metabolic abnormalities linked to critical elements of neurodegeneration. We recently administered combined metabolic activators (CMA) to the AD rat model and observed that CMA improves the AD-associated histological parameters in the animals. CMA promotes mitochondrial fatty acid uptake from the cytosol, facilitates fatty acid oxidation in the mitochondria, and alleviates oxidative stress. Methods Here, we designed a randomised, double-blinded, placebo-controlled phase-II clinical trial and studied the effect of CMA administration on the global metabolism of AD patients. One-dose CMA included 12.35 g L-serine (61.75%), 1 g nicotinamide riboside (5%), 2.55 g N-acetyl-L-cysteine (12.75%), and 3.73 g L-carnitine tartrate (18.65%). AD patients received one dose of CMA or placebo daily during the first 28 days and twice daily between day 28 and day 84. The primary endpoint was the difference in the cognitive function and daily living activity scores between the placebo and the treatment arms. The secondary aim of this study was to evaluate the safety and tolerability of CMA. A comprehensive plasma metabolome and proteome analysis was also performed to evaluate the efficacy of the CMA in AD patients. Results We showed a significant decrease of AD Assessment Scale-cognitive subscale (ADAS-Cog) score on day 84 vs day 0 (P = 0.00001, 29% improvement) in the CMA group. Moreover, there was a significant decline (P = 0.0073) in ADAS-Cog scores (improvement of cognitive functions) in the CMA compared to the placebo group in patients with higher ADAS-Cog scores. Improved cognitive functions in AD patients were supported by the relevant alterations in the hippocampal volumes and cortical thickness based on imaging analysis. Moreover, the plasma levels of proteins and metabolites associated with NAD + and glutathione metabolism were significantly improved after CMA treatment. Conclusion Our results indicate that treatment of AD patients with CMA can lead to ...
    Keywords Alzheimer’s disease ; Combined metabolic activators ; Multi-omics ; Systems biology ; Systems medicine ; Neurology. Diseases of the nervous system ; RC346-429
    Subject code 610
    Language English
    Publishing date 2023-01-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Inter-library loan at ZB MED

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