1.Efficiency and safety of haematopoietic stem cell collection in healthy donors
Rui HE ; Bangqiang ZHU ; Huiqin WEN ; Haijing WANG ; Maohong BIAN ; Yujie DIAO
Chinese Journal of Blood Transfusion 2025;38(2):209-213
[Objective] To explore the key factors affecting the efficiency and safety of hematopoietic stem cell apheresis. [Methods] The clinical data of 59 healthy donors who underwent allogeneic hematopoietic stem cell donation in the First Affiliated Hospital of Anhui Medical University from January 2021 to June 2024 were retrospectively analyzed. The number of CD34+ cells was used to evaluate the eligibility of stem cell collection. The effects of donor gender, age, patient weight, as well as the number of WBC, MNC, RBC, Hb, HCT, PLT, CD34+ cells, CD34+ percentage and instrument operating parameters on collection efficiency were analyzed. [Results] A total of 59 donors were enrolled, and 68 occasions of stem cell apheresis were performed, with a qualified collection rate of 56%. Donor gender, age, patient weight, total blood circulation volume, anticoagulant dosage, collection time, calcium gluconate dosage and RBC, Hb, HCT levels were not significantly correlated with the collection effect (P>0.05). Multivariate logistic regression analysis showed that the number of MNC cells, CD34+ cells and stem cell product volume were the key factors affecting the efficiency and safety. A total of 12 donors had mild adverse reactions during the collection process, and all of them were improved after treatment. [Conclusion] Optimizing apheresis strategy based on the three factors of MNC, WBC count and stem cell product volume on the day of collection will help to achieve high-quality collection and improve the success rate of transplantation.
2.Rosmarinic acid inhibits high glucose-induced cardiomyocyte hypertrophy by activating Parkin-mediated mitophagy.
Jiayu DIAO ; Hongmou ZHAO ; Yujie NING ; Wenqi HAN ; Yi WANG ; Gong CHENG ; Xiling SHOU ; Hongjun YOU
Journal of Southern Medical University 2020;40(11):1628-1633
OBJECTIVE:
To evaluate the effect of rosmarinic acid (RA) on mitophagy and hypertrophy of cardiomyocytes exposed to high glucose (HG).
METHODS:
Rat cardiomyocytes (H9c2) exposed to HG (25 mmol/L) were treated with 50 μmol/L RA or with both RA treatment and Parkin siRNA transfection, with the cells cultured in normal glucose (5.5 mmol/L) and HG as the controls. The expressions of PINK1, Parkin and LC3II/LC3I in the cells were detected by Western blotting. The formation of mitochondrial autophagosomes was observed by transmission electron microscope. Flow cytometry was employed to detect the level of reactive oxygen species (ROS) and apoptotic rate of the cells. The activities of respiratory chain complex enzymes were measured by spectrophotometry. Fluorescence enzyme labeling and
RESULTS:
RA treatment significantly increased the expression levels of PINK1, Parkin and LC3-II/I (
CONCLUSIONS
RA can protect rat cardiomyocytes against oxidative stress injury and cardiomyocyte hypertrophy induced by HG by activating Parkin-mediated mitophagy.
Animals
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Cinnamates
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Depsides
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Glucose
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Hypertrophy
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Mitophagy
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Myocytes, Cardiac
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Protein Kinases
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Rats
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Reactive Oxygen Species
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Ubiquitin-Protein Ligases/genetics*
3.Emodin alleviates cardiac fibrosis by suppressing activation of cardiac fibroblasts upregulating metastasis associated protein 3.
Dan XIAO ; Yue ZHANG ; Rui WANG ; Yujie FU ; Tong ZHOU ; Hongtao DIAO ; Zhixia WANG ; Yuan LIN ; Zhange LI ; Lin WEN ; Xujuan KANG ; Philipp KOPYLOV ; Dmitri SHCHEKOCHIKHIN ; Yong ZHANG ; Baofeng YANG
Acta Pharmaceutica Sinica B 2019;9(4):724-733
Excess activation of cardiac fibroblasts inevitably induces cardiac fibrosis. Emodin has been used as a natural medicine against several chronic diseases. The objective of this study is to determine the effects of emodin on cardiac fibrosis and the underlying molecular mechanisms. Intragastric administration of emodin markedly decreased left ventricular wall thickness in a mouse model of pathological cardiac hypertrophy with excess fibrosis induced by transaortic constriction (TAC) and suppressed activation of cardiac fibroblasts induced by angiotensin II (AngII). Emodin upregulated expression of metastasis associated protein 3 (MTA3) and restored the MTA3 expression in the setting of cardiac fibrosis. Moreover, overexpression of MTA3 promoted cardiac fibrosis; in contrast, silence of MTA3 abrogated the inhibitory effect of emodin on fibroblast activation. Our findings unraveled the potential of emodin to alleviate cardiac fibrosis upregulating MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis.