scholarly journals Sodium Selenite Improves The Therapeutic Effect Of BMSCs Via Promoting The Proliferation And Differentiation, Thereby Promoting The Hematopoietic Factors

2019 ◽  
Vol Volume 12 ◽  
pp. 9685-9696
Author(s):  
Dongmei Yan ◽  
Botao Tang ◽  
Lixin Yan ◽  
Lei Zhang ◽  
Meijuan Miao ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Sodium Selenite ◽  
Proliferation And Differentiation ◽  
Hematopoietic Factors

scholarly journals P044 Milk derived exosomes has a therapeutic effect on experimental colitis

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S155-S155
Author(s):  
R Golan-Gerstl ◽  
N Koroukhov ◽  
Y Elbaum Shiff ◽  
I Shilo ◽  
S Reif
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Therapeutic Effect ◽  
Experimental Colitis ◽  
Intestinal Epithelial ◽  
Mice Model ◽  
High Concentration ◽  
Fluorescent Signal ◽  
Proliferation And Differentiation

Abstract Background Inflammatory bowel disease (IBD) is a complex disorder that results from a dysregulated immune response in the gut. Emerging therapy for IBD treatment is mainly focused on regulation of the immune response. Exosomes are nanovesicle packing different molecules such as miRNAs that transfer their cargo to recipient cells. We and others found that mammalian milk contain high concentration of exosomes (milk-derived exosomes, MDE) carrying beneficial miRNAs such as miRNA-148. Furthermore, MDE are taken up by different cell type such as intestinal epithelial cells, modify target gene expression, promote proliferation and differentiation of colon epithelial cells. The aim of this study is to explore the therapeutic effect of MDE on colitis. Methods We used gavage administration of MDE labelled with DiR dye to track their localisation patterns in vivo. The therapeutic effect of MDE on colitis was study in mice model of SDS induced colitis, colon length, histopathological scoring grade, cytokine expression, stool consistency and miRNA expression were analysed. Results Imaging of mouse that have receive labelled MDE revealed an accumulation of fluorescent signal in the intestine. Moreover, fluorescent signal in the intestine and liver is time dependent. MDE reduced the histopathological scoring grade from 5.83 ± 1.47 to 0.6 ± 0.6, p < 0.05. The length of the colon of MDE-treated animals was 7.9 ± 0.19 in comparison to 6.92 ± 0.3 p < 0.05 of the untreated. The weight loss as a result of the colitis was reverted in MDE-treated mice. Likewise, MDE treatment reduced IL-6, TNF-α and caveolin expression from 3.83 to 0.78, 1.59 to 0.86 and 3.52 to 1.1, respectively. Highly expressed miRNAs (miRNA-320, 375, Let-7a and 6073) were found to be more abundant in colon of MDE treatment mice compared with the untreated. Conclusion This study demonstrated that MDE have a therapeutic effect on colitis in vivo. Proving the effect of MDE on colitis will have implications for the potential of adding MDE as a therapeutic nutrient to be included in the formulas for IBD patients.

scholarly journals Vimentin-Rab7a Pathway Mediates the Migration of MSCs and Lead to Therapeutic Effects on ARDS

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Kai Wang ◽  
Boxiang Du ◽  
Yan Zhang ◽  
Congyou Wu ◽  
Xiuli Wang ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Lung Tissue ◽  
Gene Knockout ◽  
Inflammatory Factors ◽  
Mouse Lung ◽  
Therapeutic Effects ◽  
Proliferation And Differentiation ◽  
Differentiation Status ◽  
Mouse Lung Tissue ◽  
Vimentin Gene

Acute respiratory distress syndrome (ARDS) is difficult to treat and has a high mortality rate. Mesenchymal stem cells (MSCs) have an important therapeutic effect in ARDS. While the mechanism of MSC migration to the lungs remains unclear, the role of MSCs is of great clinical significance. To this end, we constructed vimentin knockout mice, extracted bone MSCs from the mice, and used them for the treatment of LPS-induced ARDS. H&E staining and Masson staining of mouse lung tissue allowed us to assess the degree of damage and fibrosis of mouse lung tissue. By measuring serum TNF-α, TGF-β, and INF-γ, we were able to monitor the release of inflammatory factors. Finally, through immunoprecipitation and gene knockout experiments, we identified upstream molecules that regulate vimentin and elucidated the mechanism that mediates MSC migration. As a result, we found that MSCs from wild-type mice can significantly alleviate ARDS and reduce lung inflammation, while vimentin gene knockout reduced the therapeutic effect of MSCs in ARDS. Cytological experiments showed that vimentin gene knockout can significantly inhibit the migration of MSCs and showed that it changes the proliferation and differentiation status of MSCs. Further experiments found that vimentin’s regulation of MSC migration is mainly mediated by Rab7a. Rab7a knockout blocked the migration of MSCs and weakened the therapeutic effect of MSCs in ARDS. In conclusion, we have shown that the Vimentin-Rab7a pathway mediates migration of MSCs and leads to therapeutic effects in ARDS.

1428: Influence of Prostatic Epithelium on Proliferation and Differentiation of Stromal Cells

2005 ◽  
Vol 173 (4S) ◽  
pp. 387-387
Author(s):  
Quan Wu ◽  
Jian-Dang Shi ◽  
Yu Liu ◽  
Ke-Ming Wang ◽  
Helmut Klocker ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Proliferation And Differentiation ◽  
Prostatic Epithelium

Combination of Antibiotic Treatment with the Thrombin Inhibitor Recombinant Hirudin for the Therapy of Experimental Klebsiella pneumoniae Sepsis

1994 ◽  
Vol 71 (06) ◽  
pp. 768-772 ◽  
Author(s):  
Gerhard Dickneite ◽  
Jörg Czech
Keyword(s):  
Septic Shock ◽  
Klebsiella Pneumoniae ◽  
Organ Failure ◽  
Therapeutic Effect ◽  
Disseminated Intravascular Coagulation ◽  
Post Infection ◽  
Thrombin Inhibitor ◽  
Bolus Administration ◽  
Bacterial Burden ◽  
Recombinant Hirudin

SummaryRats which were infected with the gramnegative pathogen Klebsiella pneumoniae develop disseminated intravascular coagulation (DIC), multi-organ failure (MOF) and finally die in a septic shock. We investigated the therapeutic effect of antibiotic (tobramycin) treatment combined with the infusion of the highly specific thrombin inhibitor rec. hirudin. Although administration of 2 mg/kg tobramycin alone leads to a decrease of the bacterial burden, DIC could not be prevented. Infusion of rec. hirudin (0.25 mg/kg x h) for 4 h (start of treatment 1 h post infection), in addition to a bolus administration of tobramycin, led to an amelioration of DIC parameters as fibrinogen, thrombin-antithrombin complex (TAT) and platelets. Serum transaminase levels (GOT, GPT) as a marker of MOF were significantly improved by rec. hirudin, the T50 value increased from 17 h in the tobramycin group to 42 h in the tobramycin + rec. hirudin giuup, muilality rates were 90% or 60%, respectively. Combination of heparin (10011/kg x h) and tobramycin was not effective on survival.

Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease

2020 ◽  
Vol 3 (2) ◽  
pp. 216-242 ◽  
Author(s):  
Mayuri Shukla ◽  
Areechun Sotthibundhu ◽  
Piyarat Govitrapong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Adult Neurogenesis ◽  
Adult Brain ◽  
Therapeutic Approaches ◽  
Therapeutic Implications ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Progenitor Cell Proliferation

The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.   

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