1.Mechanism of mitochondrial oxidative phosphorylation disorder in male infertility.
Kai MENG ; Qian LIU ; Yiding QIN ; Wenjie QIN ; Ziming ZHU ; Longlong SUN ; Mingchao JIANG ; Joseph ADU-AMANKWAAH ; Fei GAO ; Rubin TAN ; Jinxiang YUAN
Chinese Medical Journal 2025;138(4):379-388
Male infertility has become a global concern, accounting for 20-70% of infertility. Dysfunctional spermatogenesis is the most common cause of male infertility; thus, treating abnormal spermatogenesis may improve male infertility and has attracted the attention of the medical community. Mitochondria are essential organelles that maintain cell homeostasis and normal physiological functions in various ways, such as mitochondrial oxidative phosphorylation (OXPHOS). Mitochondrial OXPHOS transmits electrons through the respiratory chain, synthesizes adenosine triphosphate (ATP), and produces reactive oxygen species (ROS). These mechanisms are vital for spermatogenesis, especially to maintain the normal function of testicular Sertoli cells and germ cells. The disruption of mitochondrial OXPHOS caused by external factors can result in inadequate cellular energy supply, oxidative stress, apoptosis, or ferroptosis, all inhibiting spermatogenesis and damaging the male reproductive system, leading to male infertility. This article summarizes the latest pathological mechanism of mitochondrial OXPHOS disorder in testicular Sertoli cells and germ cells, which disrupts spermatogenesis and results in male infertility. In addition, we also briefly outline the current treatment of spermatogenic malfunction caused by mitochondrial OXPHOS disorders. However, relevant treatments have not been fully elucidated. Therefore, targeting mitochondrial OXPHOS disorders in Sertoli cells and germ cells is a research direction worthy of attention. We believe this review will provide new and more accurate ideas for treating male infertility.
Male
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Humans
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Infertility, Male/metabolism*
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Oxidative Phosphorylation
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Mitochondria/metabolism*
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Spermatogenesis/physiology*
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Sertoli Cells/metabolism*
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Oxidative Stress/physiology*
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Animals
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Reactive Oxygen Species/metabolism*
2.Critical role of mitochondrial dynamics in chronic respiratory diseases and new therapeutic directions.
Xiaomei WANG ; Ziming ZHU ; Haocheng JIA ; Xueyi LU ; Yingze ZHANG ; Yingxin ZHU ; Jinzheng WANG ; Yanfang WANG ; Rubin TAN ; Jinxiang YUAN
Chinese Medical Journal 2025;138(15):1783-1793
Chronic obstructive pulmonary disease (COPD) and pulmonary hypertension (PH) are both chronic progressive respiratory diseases that cannot be completely cured. COPD is characterized by irreversible airflow limitation, chronic airway inflammation, and gradual decline in lung function, whereas PH is characterized by pulmonary vasoconstriction, remodeling, and infiltration of inflammatory cells. These diseases have similar pathological features, such as vascular hyperplasia, arteriolar contraction, and inflammatory infiltration. Despite these well-documented observations, the exact mechanisms underlying the occurrence and development of COPD and PH remain unclear. Evidence that mitochondrial dynamics imbalance is one major factor in the development of COPD and PH. Mitochondrial dynamics is precisely regulated by mitochondrial fusion proteins and fission proteins. When mitochondrial dynamics equilibrium is disrupted, it causes mitochondrial and even cell morphological dysfunction. Mitochondrial dynamics participates in various pathological processes for heart and lung disease. Mitochondrial dynamics may be different in the early and late stages of COPD and PH. In the early stages of the disease, mitochondrial fusion increases, inhibiting fission, and thereby compensatorily increasing adenosine triphosphate (ATP) production. With the development of the disease, mitochondria decompensation causes excessive fission. Mitochondrial dynamics is involved in the development of COPD and PH in a spatiotemporal manner. Based on this understanding, treatment strategies for mitochondrial dynamics abnormalities may be different at different stages of COPD and PH disease. This article will provide new ideas for the potential treatment of related diseases.
Humans
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Mitochondrial Dynamics/physiology*
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Pulmonary Disease, Chronic Obstructive/metabolism*
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Hypertension, Pulmonary/metabolism*
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Mitochondria/metabolism*
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Animals
3.Optimization of molding process of Jinpuju Qingrelishi Granules by Response Surface Methodology
Weiwei CHEN ; Jincheng HUANG ; Jinxiang LI ; Ying QIN ; Yuyang LI ; Xiangcen LIU ; Xinggui TAN
International Journal of Traditional Chinese Medicine 2022;44(11):1273-1277
Objective:To optimize the best molding process of Jinpuju Qingrelishi Granules.Methods:Based on the single factor test, the relative density of clear ointment and the amount of diluent (dextrin∶lactose=2∶1) are used as investigating factors, and the overall evaluation of the molding rate and angle of repose overall desirability (OD) is used as the evaluation index. The effect surface method is used to optimize the best molding process of Jinpuju Qingrelishi Granules.Results:The best molding process conditions: the relative density of the clear paste is 1.20 (60 ℃) and the amount of diluent is 3 times that of the clear paste. After mixing the clear paste and diluent, make soft material, pass through a 14-mesh sieve to granulate, dry in an oven (55 ℃) for 1 hour, and sizing to obtain. The molding rates of the three batches of verification test granules were 93.73%, 93.03%, 95.59%, respectively, the predicted OD value was 0.928, the verification value was 0.936, and the deviation from the predicted value was -0.86%.Conclusion:The molding process of this experiment is stable and reliable, with good repeatability, which can provide a reference for the follow-up research of Jinpuju Qingrelishi Granules.
4.Study on the Chemical Constituents in the Chloroform Extract of Fructus Canarii
Luoping YANG ; Han MENG ; Suiyi TAN ; Jinxiang CHEN ; Wenjun DUAN
China Pharmacy 2018;29(10):1340-1343
OBJECTIVE:To study the chemical constituents in the chloroform extract of Fructus Canarii. METHODS:The chloroform extract of Fructus Canarii was isolated and purified by MCI,Toyopearl HW-40F,reverse-phase C18,Sephadex LH-20 column. The structure of compounds was analyzed and identified by physicochemical properties and spectral data(mass spectrum, hydrogen spectrum and carbon spectrum). RESULTS:Eight compounds were isolated from chloroform extract of Fructus Canarii, namely Dihydrophaseicacid-3′-O-β-D-glucopyranoside(1),3,4-Dihydroxybenzoic acid(2),3-O-galloylquinic acid(3),Gallic acid (4), Ethyl gallate(5), Scopoletin(6), Dllagic acid-4-O-α-L-rhamnopyranoside(7) and Isocorilagin(8). CONCLUSIONS:Compounds 1,2 and 7 were firstly obtained from Fructus Canarii. The study lays foundation for quality evaluation of Fructus Canarii.
5.Matrix metalloproteinases-11 collabrotive matrix metalloproteinases-14 promote development of breast carcinoma
Hongyan HUANG ; Jinxiang TAN ; Guosheng REN
Chinese Journal of Immunology 2016;32(7):996-999
Objective:To investigate the expression pattern of MMP-11 and MMP-14 in breast carcinoma, and the effect of MMP-11 on breast carcinoma cell migration and invasion. Methods:MMP-11 and MMP-14 expression were examined in 161 invasive breast carcinoma tissue samples and 10 normal breast tissue samples. siRNA was used to knockout MMP-11 in breast carcinoma cell line MB-231 and Transwells were used to evaluate changes in migration ability and invasion ability. Results:Both MMP-11 and MMP-14 were highly expressed in breast carcinoma samples,122 and 149 samples out of 161,respectively. The expression of both proteins were correlated with lymph node metastasis and TNM staging. After knockout of MMP-11,the expression of both proteins decreased in MB-231 cell line and experiments show that the cell′s migration and invasion abilities were significantly weakened. Conclusion:MMP-11 and MMP-14 could promote invasion and metastasis of breast carcinoma. Knockout of MMP-11 results in the downregulated expression of MMP-14,and the inhibition of breast carcinoma cell′s migration and invasion. They could be potential prognostic markers and treatment targets for of breast carcinoma.
6.miR-197 Expression in Peripheral Blood Mononuclear Cells from Hepatitis B Virus-Infected Patients.
Li CHEN ; Congzhi LI ; Zaiquan PENG ; Jinxiang ZHAO ; Guozhong GONG ; Deming TAN
Gut and Liver 2013;7(3):335-342
BACKGROUND/AIMS: This study aimed to investigate the microRNA (miRNA) expression profiles in peripheral blood mononuclear cell (PBMC) of hepatitis B virus (HBV)-infected patients with different clinical manifestations and to analyze the function of miR-197. METHODS: PBMC miRNA expression profiles in 51 healthy controls, 70 chronic asymptomatic carriers, 107 chronic hepatitis B patients, and 76 HBV-related acute on chronic liver failure patients were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). miR-197 mimic and inhibitor were transfected in THP-1 cells. qRT-PCR and ELISA for interleukin (IL)-18 mRNA and protein levels were performed, respectively. RESULTS: The microarray analysis revealed that 17 PBMC miRNA expression profiles (12 miRNAs downregulated and five miRNAs upregulated) differed significantly in HBV-induced liver disease patients presenting with various symptoms. The qRT-PCR results suggested that the PBMC miR-197 levels regularly decreased as the severity of liver disease symptoms became aggravated. IL-18, a key regulator in inflammation and immunity, was inversely correlated with miR-197 levels. Bioinformatic analysis indicated that IL-18 was a target of miR-197. Exogenous expression of miR-197 could significantly repress IL-18 expression at both the mRNA and protein levels in THP-1 cells. CONCLUSIONS: We concluded that multiple PBMC miRNAs had differential expression profiles during HBV infection and that miR-197 may play an important role in the reactivation of liver inflammation by targeting IL-18.
End Stage Liver Disease
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Enzyme-Linked Immunosorbent Assay
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Hepatitis
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Hepatitis B
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Hepatitis B virus
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Hepatitis B, Chronic
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Humans
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Hydrazines
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Inflammation
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Interleukin-18
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Interleukins
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Liver
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Liver Diseases
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Liver Failure
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Microarray Analysis
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MicroRNAs
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Real-Time Polymerase Chain Reaction
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RNA, Messenger
7.The effect of shRNA-CXCR4 on breast cancer cell growth and proliferation in vitro
Hongyuan LI ; Guosheng REN ; Jinxiang TAN
China Oncology 2006;0(12):-
Background and purpose:A chemokine receptor,CXCR4,and its endogenous ligand,stromal cell-derived factor-1(SDF-1),have been recognized to be involved in the invasion and metastasis of cancer.Inhibition of CXCR4 may be a new therapeutic target.We studied whether shRNA-CXCR4 could inhibit the CXCR4 gene expression and the proliferation in MCF-7,MDA-MB-231 and MDA-MB-435s breast cancer cells.Methods:Through knockdown CXCR4 by shRNA,the CXCR4 mRNA expression was detected by RT-PCR and the CXCR4 protein expression was mesured by Western blot.The proliferation of breast cancer cells was evaluated by MTT and flow cytometry.Results:The CXCR4mRNA and its protein expression decreased significantly in MCF-7(the average level of CXCR4 mRNA and protein expression were 0.089,0.177 in PG-CXCR4 group,compared with 0.327 and 0.313 for mRNA expression,0.911,0.874 for protein expression in control and PG-HK group),MDA-MB-231(the average level of CXCR4 mRNA and protein expression were 0.152 and 0.153 in PG-CXCR4 group,compared with 0.40 and 0.45 for mRNA expression,0.829 and 0.878 for protein expression in control and PG-HK group)and MDA-MB-435s(the average level of CXCR4 mRNA and protein expression were 0.198 and 0.173 in PG-CXCR4 group,compared with 0.69 and 0.77 for mRNA expression,0.877 and 0.906 for protein expression in control and PG-HK group)breast cancer cells(P
8.Silencing breast cancer cell CXCR4 gene in vitro
Hongyuan LI ; Guosheng REN ; Jinxiang TAN
Journal of Third Military Medical University 2003;0(08):-
Objective To study whether shRNA-CXCR4 could inhibit the CXCR4 gene expression in MCF-7,MDA-MB-231 and MDA-MB-435s breast cancer cells.Methods After the knockdown of CXCR4 by shRNA,the CXCR4 mRNA expression by RT-PCR and the CXCR4 protein expression by Western blotting in breast cancer cells were examined.Results The CXCR4 mRNA expression and its protein expression were decreased significantly in MCF-7,MDA-MB-231 and MDA-MB-435s breast cancer cells by shRNA-CXCR4(P
9.Effects of HYAL1 gene overexpression on invasive,angiogenic and proliferative ability of breast cancer cells
Xinliang SU ; Guosheng REN ; Xiaoyi WANG ; Jinxiang TAN
Journal of Third Military Medical University 2003;0(15):-
Objective To study the effects of HYAL1 gene overexpression on invasive, angiogenic and proliferative ability of breast cancer cell lines MCF-7 and ZR-75-30. Methods Double-chamber co-culture technique was applied to construct the invasive model and angiogenic model in vitro, which was used to detect the invasive and angiogenic potential of breast cancer cell; MTT and flow cytometry were used to detect the proliferation of breast cancer cells. Results Breast cancer cells overexpressing HYAL1 gene showed stronger invasive potential and angiogenic potential than control cells, but had no significant difference on proliferative potential. Conclusion Overexpression of HYAL1 gene can promote the invasion and angiogenesis of breast cancer cells in vitro, but not affect the proliferation.
10.Effect of silencing hyaluronidase gene HYAL1 by RNA interference on invasive potential of human breast cancer cell lines
Jinxiang TAN ; Xiaoyi WANG ; Guosheng REN ; Gang TU ; Xiaotao LI ; Liang RAN
Chinese Journal of General Surgery 2000;0(12):-
Objective To study the effect of RNA interference (RNAi) on HYAL1 gene mRNA expression and the invasive potential of human breast cancer cell lines. Methods Chemically synthesized double stranded RNA (dsRNA) targeting HYAL1 was transfected into human breast cancer cell lines MDA-MB-231, MDA-MB453S, ZR-75 and ZR-75-30 using SiPORT Lipid. The transfection efficiency was observed under fluorescence confocal microscopy. Expression of HYAL1 mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). Cell penetrate matrigel capacity were determined by in vitro experiment. Results HYAL1 -siRNA effectively inhibited HYAL1 mRNA expression ( P

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