Biochemical and Molecular Mechanisms of Platelet-Rich Plasma in Ameliorating Liver Fibrosis Induced by Dimethylnitrosurea

Salem, Neveen A.; Hamza, Amal H.; Alnahdi, Hanan S.; Ayaz, Najla O.

doi:10.1159/000491544

Cited by 31 publications

(27 citation statements)

References 28 publications

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“…Afterwards Jezequel and coworkers conducted a pioneering study on various aspects of NDMA-induced hepatic fibrosis with special emphasis to pathophysiology and immunohistochemistry and demonstrated that it is a good and reproducible animal model, and appropriate for the study of the early events associated with the development of hepatic fibrosis 48–52 . Furthermore, the model has been employed recently to investigate various aspects of the molecular pathogenesis of hepatic fibrosis and to study therapeutic approaches including the arrest of activation of stellate cells 53–60 . Over the last 20 years, we have extensively studied various biochemical and pathophysiological aspects of the pathogenesis of NDMA-induced hepatic fibrosis in rats and mice involving glycoprotein metabolism 17 , collagen biosynthesis and metabolism 4–6 , LDH isoenzymes 61 , biochemical abnormalities 62 , oxidative stress and osteopontin 10,63–65 , hyaluronic acid and hyaluronidase 66,67 , mineral and trace element metabolism 68–70 , antioxidants 10,71,72 and gene therapy 13,73,74 , lysosomal fragility 75,76 , and the role of metalloproteinases 14,77,78 .…”

Section: N-nitrosodimethylamine-induced Hepatic Fibrosis and Liver CImentioning

confidence: 99%

Molecular mechanisms in the pathogenesis of N-nitrosodimethylamine induced hepatic fibrosis

2019

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Hepatic fibrosis is marked by excessive synthesis and deposition of connective tissue proteins, especially interstitial collagens in the extracellular matrix of the liver. It is a result of an abnormal wound healing in response to chronic liver injury from various causes such as ethanol, viruses, toxins, drugs, or cholestasis. The chronic stimuli involved in the initiation of fibrosis leads to oxidative stress and generation of reactive oxygen species that serve as mediators of molecular events involved in the pathogenesis of hepatic fibrosis. These processes lead to cellular injury and initiate inflammatory responses releasing a variety of cytokines and growth factors that trigger activation and transformation of resting hepatic stellate cells into myofibroblast like cells, which in turn start excessive synthesis of connective tissue proteins, especially collagens. Uncontrolled and extensive fibrosis results in distortion of lobular architecture of the liver leading to nodular formation and cirrhosis. The perpetual injury and regeneration process could also results in genomic aberrations and mutations that lead to the development of hepatocellular carcinoma. This review covers most aspects of the molecular mechanisms involved in the pathogenesis of hepatic fibrosis with special emphasize on N -Nitrosodimethylamine (NDMA; Dimethylnitorsmaine, DMN) as the inducing agent.

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Section: N-nitrosodimethylamine-induced Hepatic Fibrosis and Liver CImentioning

confidence: 99%

Molecular mechanisms in the pathogenesis of N-nitrosodimethylamine induced hepatic fibrosis

2019

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“…TGF-β is one of the main drivers of fibrosis. Because PRP has shown an antifibrotic potential in epidural and liver fibrosis, 24,46 how TGF-β in PRP affects the fibrosis stage of AC is still controversial. Fourth, the stage of disease may vary among patients; however, the stage could be regarded as freezing or inflammatory in that most of the patients had unmanageable pain that was mainly associated with inflammation.…”

Section: Discussionmentioning

confidence: 99%

Allogenic Pure Platelet-Rich Plasma Therapy for Adhesive Capsulitis: A Bed-to-Bench Study With Propensity Score Matching Using a Corticosteroid Control Group

Lee

Yoon

et al. 2021

Am J Sports Med

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Background: While platelet-rich plasma (PRP) has been widely studied for musculoskeletal disorders, few studies to date have reported its use for adhesive capsulitis (AC). Fully characterized and standardized allogenic PRP may provide clues to solve the underlying mechanism of PRP with respect to synovial inflammation and thus may clarify its clinical indications. Purpose: To clinically evaluate the safety and efficacy of a fully characterized pure PRP injection in patients with AC and to assess the effects of pure PRP on synoviocytes with or without inflammation in vitro. Study Design: Controlled laboratory study and cohort study; Level of evidence, 3. Methods: For the clinical analysis, a total of 15 patients with AC received an ultrasonography-guided intra-articular PRP injection and were observed for 6 months. Pain, range of motion (ROM), muscle strength, shoulder function, and overall satisfaction in the patients were evaluated using questionnaires at 1 week as well as at 1, 3, and 6 months after the PRP injection and results were compared with the results of a propensity score−matched control group that received a corticosteroid injection (40 mg triamcinolone acetonide). For the in vitro analysis, synoviocytes were cultured with or without interleukin-1β (IL-1β) and PRP. The gene expression of proinflammatory and anti-inflammatory cytokines as well as matrix enzymes and their inhibitors was evaluated. Results: At 6-month follow-up, pure PRP significantly decreased pain and improved ROM, muscle strength, and shoulder function to levels comparable with those after a corticosteroid injection. All pain values, strength measurements, and functional scores significantly improved up to 6 months in the PRP group, but these measures improved up to 3 months and then were decreased at 6 months in the corticosteroid group. ROM was significantly improved in the 2 groups at 6 months compared with baseline. Allogenic PRP did not cause adverse events. For the in vitro findings, PRP induced inflammation but significantly improved the IL 1β−induced synovial inflammatory condition by decreasing proinflammatory cytokines such as IL-1β, tumor necrosis factor−α, IL-6, cyclooxygenase-2, and microsomal prostaglandin E synthase−1 and decreased matrix enzymes (matrix metalloproteinase−1, −3, and −13 as well as a disintegrin and metalloproteinase with thrombospondin motifs−4 and −5) and further increasing anti-inflammatory cytokines such as vasoactive intestinal peptide. Conclusion: This study showed that PRP decreased pain and improved shoulder ROM and function to an extent comparable with that of a corticosteroid in patients with AC. Allogenic pure PRP acted in a pleiotropic manner and decreased proinflammatory cytokines only in the inflammatory condition. Clinical Relevance: Allogenic PRP could be a treatment option for the inflammatory stage of AC.

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“…No previous study was associated with the effect of PRP on the liver. Salem et al described the regenerative impact of platelets in the liver of adult male Wistar rats, which comprises three pathways: a direct impact on hepatocytes, a favorable impact on liver sinusoidal endothelial cells, and a collaborative impact on Kupffer cells [29]. Therefore, it was proposed that the expansion of platelets induced by platelet transfusion would enhance liver functions in patients with chronic liver diseases in the clinical setting [30].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Submucosal Injection of Plasma-Rich Platelets on Blood Inflammatory Markers for Patients with Bimaxillary Protrusion Undergoing Orthodontic Treatment

Mahmood

Chawshli

2019

International Journal of Inflammation

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Objectives The present study aims to reveal the systemic effects of submucosal injection of plasma-rich platelets (PRP) on blood inflammatory markers which was used in an attempt to reduce the retraction time of the upper canine following extraction of upper maxillary premolars for patients with bimaxillary protrusion. Hypothesis No change on comparing the values of blood inflammatory markers before and after submucosal injection of PRP. Methods Eighteen female patients with bimaxillary protusion were selected from patients seeking orthodontic treatment from the College of Dentistry/University of Sulaimai, whose maxillary and mandibular first premolars were decided to be extracted after proper diagnosis. Thirty-three blood markers (twenty hematological and thirteen biochemical markers) were estimated before orthodontic bracketing, 24 hours and 7 days following submucosal injection of PRP (5 cc) to reveal the systematic effect of PRP on blood inflammatory markers that were used in an attempt to reduce the retraction time of the upper canine following extraction of upper maxillary premolars for patients with bimaxillary protrusion. Results The results indicate nonsignificant differences in the values of all blood markers except for gamma GT (GGT), PDWa, serum albumin, serum total protein, and total calcium. Gamma level significantly increased for both test intervals. On the other hand, there was a significant drop in the value of PDWa while for alkaline phosphatase, there was a drop within the first 24 hr of PRP injection while after 7 days the value was significantly increased. On the other hand, there was a drop in the level of serum albumin, while there was an increase in the serum total protein and total calcium. Conclusion Submucosal injection of PRP could lead to systematic alteration of blood parameters including ALK phosphatase, gamma GT, serum albumin, and serum total protein, which may be related to liver function in addition to increase in the level of PDWa and serum calcium. We present evidence that PRP contains and may trigger systemic effect. Thus, further investigation is recommended to follow up the patient for a longer period of time and on a larger sample. This trial is registered with U1111-1221-8829 by Sri Lanka Clinical Trial Registry, SLCTR/2018/040, and No. 64 on 6th August 2018 at the local clinical studies database, College of Dentistry.

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Biochemical and Molecular Mechanisms of Platelet-Rich Plasma in Ameliorating Liver Fibrosis Induced by Dimethylnitrosurea

Cited by 31 publications

References 28 publications

Molecular mechanisms in the pathogenesis of N-nitrosodimethylamine induced hepatic fibrosis

Molecular mechanisms in the pathogenesis of N-nitrosodimethylamine induced hepatic fibrosis

Allogenic Pure Platelet-Rich Plasma Therapy for Adhesive Capsulitis: A Bed-to-Bench Study With Propensity Score Matching Using a Corticosteroid Control Group

The Effect of Submucosal Injection of Plasma-Rich Platelets on Blood Inflammatory Markers for Patients with Bimaxillary Protrusion Undergoing Orthodontic Treatment

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