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According to the World Health Organization's world report on hearing, nearly 2.5 billion people worldwide will suffer from hearing loss by 2050, which may contribute to a severe impact on individual life quality and national economies. Sensorineural hearing loss (SNHL) occurs commonly as a result of noise exposure, aging, and ototoxic drugs, and is pathologically characterized by the impairment of mechanosensory hair cells of the inner ear, which is mainly triggered by reactive oxygen species accumulation, inflammation, and mitochondrial dysfunction. Though recent advances have been made in understanding the ability of cochlear repair and regeneration, there are still no effective therapeutic drugs for SNHL. Chinese herbal medicine which is widely distributed and easily accessible in China has demonstrated a unique curative effect against SNHL with higher safety and lower cost compared with Western medicine. Herein we present trends in research for Chinese herbal medicine for the treatment of SNHL, and elucidate their molecular mechanisms of action, to pave the way for further research and development of novel effective drugs in this field.
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Air pollution is a global issue that threatens human health. In recent years, more and more studies have found that air pollution is closely related to the occurrence of depression. As a serious neuropsychiatric disorder whose incidence is rising rapidly year by year, depression has become an invisible killer of public health. At present, studies on the correlation between air pollution and depression are still very limited, and the underlying molecular mechanisms by which air pollution affects depression are not clear. Based on existing epidemiological and toxicological studies, this paper provided a review of the relationship between air pollution and depression and the possible biological mechanisms, with a focus on the relationship between air pollution and depression indicators and the possible factors affecting depression such as types of air pollutants, exposure time, age and health status of study subjects. In addition, the potential roles of neuroinflammation, oxidative stress, neurogenesis, and apoptosis in the process of air pollution-induced depression were also discussed in order to provide a scientific basis for the prevention and treatment of air pollution-induced depression.
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Cholesterol metabolism is a hot topic in exploration of cancer treatment in recent years,and its complex mechanism of action potentially lays a molecular foundation related to lipid-cancer.However,most studies focus only on cholesterol as a product to understand and analyze the progress of cancer,ignoring the phased effects of related derivatives,regulatory proteins and immune cells in its metabolic process,so whether to find targets to regulate colorectal cancer(CRC)from the cholesterol metabolic pathway has become a research focus.This paper reviews the molecular mechanism and the role of signaling pathways in metabolic reprogramming of CRC starting from the abnormal intracellular cholesterol metabolic pathway in order to provide new ideas for the targeted cholesterol therapy of CRC.
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Narciclasine(NCS),a hymenocallis littoralis alkaloid extracted from the bulbs of the genus Narcissus in the Lycoriaceae family,has been proven to have significant anti-tumor activity against a variety of tumor cells.The antitumor mechanisms of NCS are diverse and NCS exhibits antitumor effects through different pathways,which adapts to the current trend of developing multi-target anti-tumor drugs.This review introduces the research progress of the anti-tumor activity and mechanism of NCS in recent years based on the inhibitory effect of NCS on gastric cancer cells,oral cancer cells,polymorphous glioblastoma cells,colon cancer cells,breast cancer cells,melanoma cells and primary exudative lymphoma cells,aiming to provide ideas and references for the research and development,and design of NCS type anti-tumor drugs in the future.
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BACKGROUND:Graphene is the thinnest,strongest,and toughest type of two-dimensional new crystal material,demonstrating significant advantages in biomedical applications.Angiogenesis and vascularization of bone are key factors in tissue repair and regeneration,and are effective ways to address vascular and osteogenic issues. OBJECTIVE:To review the characteristics and mechanisms of graphene and its derivatives in promoting angiogenesis activity and vascularizing bone,in order to provide a reference for their clinical application in vascular tissue repair and regeneration. METHODS:Using a computer to search for relevant literature included in PubMed,ScienceDirect,CNKI,and Wanfang databases,the Chinese search terms were"grapheme","angiogenesis,vascularization","vascularized bone",and"endothelial cells",while the English search terms were"graphene""angiogenesis OR vascularization""vascularized bone""endothelial cells".After excluding literature unrelated to the topic of the article,according to the inclusion and exclusion criteria,62 articles were ultimately included for result analysis. RESULTS AND CONCLUSION:(1)At present,graphene oxide has been studied more and is the most widely used in graphene and its derivatives.(2)Graphene and its derivatives are suitable for heart,bone,nerve,and wound healing related diseases.(3)Graphene and its derivatives have excellent physical and chemical properties and biological properties,but they have potential cytotoxicity.We should pay attention to its biological safety in application.(4)The application of graphene and its derivatives requires further research to demonstrate the optimal size and concentration and measures to reduce toxicity.(5)On the cellular level,graphene and its derivatives can promote angiogenic activity by tip endothelial cell phenotype,mesenchymal stem cell adhesion and proliferation, and vascular smooth muscle cell growth.(6)On the molecular level,graphene and its derivatives can increase the expression of vascular endothelial growth factor,basic fibroblast growth factor,hepatocyte growth factor and activate reactive oxygen species/nitric oxide synthase/nitric oxide signaling pathway,lysophosphatilate R6/Hippo-YAP pathway,stromal cell-derived factor-1/vascular endothelial growth factor and ZEB 1/Notch1 pathway.(7)Grapheme oxide and graphene oxide-copper phosphorylated extracellular regulatory protein kinase and activated hypoxia-inducible factor-1,thereby promoting the up-regulation of vascular endothelial growth factor and bone morphogenetic protein-2 expression,and promoting angiogenesis and vascularized bone.(8)In summary,graphene and its derivatives,especially graphene oxide,have great application prospects in the repair and regeneration of vascularized tissues due to their excellent biological properties,good angiogenesis and vascularized bone ability.
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BACKGROUND:Increasing studies have found that estrogen has a certain correlation with tendinopathy,but for a long time,there are few experiments and summaries of estrogen in tendinopathy,which makes it difficult for specialists and scholars in related fields to fully understand the research status. OBJECTIVE:To summarize the current clinical or preclinical original research,so as to summarize the role of estrogen in tendinosis,and make a certain prospect for the evaluation and management of estrogen in tendinosis in the future. METHODS:Relevant literature in PubMed,Web of Science,CNKI,WanFang,and VIP databases were searched by computer.Search time was from January 2008 to September 2023.The search terms were"oestrogen,estrogen,estrogen receptor,tendinopathy,tendonopathy,sinew,tendon,tendons,myotenositis"in English and"estrogen,estrogen receptor,tendinosis,tendon,tendinitis"in Chinese.According to the selection criteria,the search results were screened and excluded,and finally 60 documents were included for review and analysis. RESULTS AND CONCLUSION:In vivo studies have shown that estrogen can promote tendon anabolism.In vitro experiments have also proved that various estrogens can promote the proliferation of tendon cells and reduce inflammation and apoptosis,but most of the experiments are limited to animal models.Estrogen receptor β acts more in tendon injury and repair processes,but estrogen receptor α has not been found to have a major impact on tendon injury.The expression of estrogen receptor β can repair the tendon by affecting the formation of fat,the deposition of type I collagen and reducing the apoptosis of tendon cells,while its over-expression may promote inflammation and angiogenesis,thus promoting the inflammatory process and playing a role in tendon injury.Animal studies have shown that estrogen deficiency may reduce the synthesis efficiency of collagen in the tendon,decrease the elasticity of tendon,inhibit the synthesis and metabolism of the tendon,which is not conducive to the repair of tendon injury,while normal level of estrogen may stimulate the synthesis of type I collagen in tendon and promote the proliferation and metabolism of tendon cells.At present,the molecular mechanism of estrogen in tendon injury has not been fully explained.More experiments focus on tendon collagen synthesis,cell proliferation and apoptosis.Only a few documents have studied the molecular mechanisms of estrogen receptor β deficiency regulating interferon regulatory factor 5-chemokine ligand 3 axis,E2 regulating estrogen receptor α and PI-3K-Akt signaling pathways,and high levels of estradiol reducing the level of free-circulating insulin-like growth factor.Various estrogens,including endogenous estrogens and phytoestrogens,are beneficial to the repair of tendinopathy at normal levels,and estrogen receptor β mainly affects the formation of fat,the deposition of type I collagen and the reduction of apoptosis of tendon cells through,which lays a foundation for the future treatment of tendinopathy with different subtypes of estrogens in vivo and the influence of estrogen membrane receptors on tendinopathy.
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Cognitive dysfunction caused by blast traumatic brain injury (bTBI) is a serious neurological disease with high incidence, serious condition and poor prognosis. bTBI can lead to a series of symptoms such as short-term memory loss, inattention or multi-tasking difficulties. In severe cases, bTBI can develop into Alzheimer′s disease, which has a great impact on patients′ normal work and life. At present, researches on cognitive dysfunction caused by bTBI mainly involve model construction, pathogenesis, pathophysiological changes, diagnosis and treatment, etc., and the molecular mechanism of its occurrence remains to be further studied. Under normal physiological conditions, the release of excitatory and inhibitory neurotransmitters, the release and uptake of Ca 2+, oxidation and antioxidant systems, and the promotion and inhibition of apoptosis are in a dynamic balance. bTBI disturbs the balance, which will lead to the damage of nerve cells at the molecular level, thus resulting in the occurrence of cognitive dysfunction. To this end, the authors summarized the aspects of excitatory toxicity and Ca 2+homeostasis disorder, oxidative stress, inflammation and edema, apoptosis, etc., and reviewed the research progress on the molecular mechanism of cognitive dysfunction caused by bTBI, so as to provide a reference for the treatment and rehabilitation of cognitive dysfunction in patients with bTBI.
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ObjectiveTo explore the molecular mechanism of Qidi Tangshen prescription （QDTS） in regulating podocyte pyroptosis in diabetes nephropathy （DN）. MethodThrough in vivo experiment， db/db mice were divided into the model group， QDTS group （3.34 g·kg-1）， valsartan capsule group （10.29 mg·kg-1）， with db/m mice serving as the normal control. Each group consisted of 8 mice， and they underwent continuous intervention for 8 weeks. After the last administration， mice were euthanized， and kidney pathological changes were observed. Additionally， the expression levels of pyroptosis-related indicators， including NOD-like receptor protein 3 （NLRP3）， Gasdermin D protein （GSDMD）， and interleukin-1β （IL-1β） protein， were examined. Through in vitro experiment， mouse podocytes were divided into the normal glucose group （5.5 mmol·L-1 glucose）， high glucose group （35 mmol·L-1 glucose）， DMSO group （35 mmol·L-1 glucose+200 mg·L-1 DMSO）， and QDTS group （35 mmol·L-1 glucose+200 mg·L-1 QDTS freeze-dried powder）. After 48 hours of intervention， the expression levels of NLRP3， GSDMD， and IL-1β proteins were measured in podocytes. A drug-ingredient-target-disease interaction network for QDTS in the treatment of DN was constructed by network pharmacology methods. The key signaling pathways regulating podocyte pyroptosis were analyzed， and validation was conducted through in vivo and in vitro experiments. ResultCompared with normal group， glomerular hyperplasia and glomerular basement membrane thickening were observed in model group， and some segments were accompanied by obvious podocellular process fusion. The protein expressions of NLRP3， GSDMD and IL-1β in mouse kidney were increased， the protein expressions of mitogen-activated protein kinase 14 （MAPK14）， V-Rel reticuloendotheliosis virus oncogene homology A （RELA） and Caspase-8 in mouse kidney were increased （P<0.05）. Compared with model group， kidney pathological injury of mice in QDTS group was significantly reduced， and the expressions of NLRP3， GSDMD and IL-1β in kidney of mice in QDTS group and valsartan group were decreased （P<0.05）. The protein expressions of MAPK14， RELA and Caspase-8 in kidney of mice in QDTS group and valsartan group were decreased （P<0.05）. Network pharmacology results showed that there were 16 targets for QDTS to regulate DN cell pyrodeath， among which MAPK14， RELA and Caspase-8 were the key targets. Compared with normal glucose group， the protein expressions of NLRP3， GSDMD and IL-1β in high glucose group were increased （P<0.05）， and the protein expressions of MAPK14， RELA and Caspase-8 in mouse podocytes were increased （P<0.05）. Compared with high glucose group， the expressions of NLRP3， GSDMD and IL-1β in podocytes of mice in QDTS group were decreased （P<0.05）， and the expressions of MAPK14， RELA and Caspase-8 in podocytes of mice in QDTS group were decreased （P<0.05）. ConclusionQDTS reduces damage to DN podocytes， which is associated with its regulation of the MAPK14/RELA/Caspase-8 signaling pathway and inhibition of podocyte pyroptosis.
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ObjectiveThis study aimed at conducting retrospective analysis of the clinical symptoms and genetic mutations in 20 children with Gitelman syndrome treated at the Affiliated Children′s Hospital of Nanjing Medical University from August 2015 to November 2022 and also explored the molecular mechanism of the pathogenic high-frequency mutation D486N in the Chinese population.MethodsWe collected the clinical manifestations, growth and development status, laboratory examination results, and SLC12A3 gene variations of the patients. We distinguished the wild-type and mutant SLC12A3 genes overexpressed in human embryonic kidney 293T cells (HEK293T). We used protein immunoblotting to detect the expression level of NCC, and used immunofluorescence techniques to examine the subcellular localization of NCC. In addition, we investigated the impact of the high-frequency SLC12A3 gene mutation D486N on NCC protein expression and localization.ResultsIn the 20 patients with Gitelman syndrome, all of them had hypokalemia. We indemnified twenty-six SLC12A3 gene mutations, 13 of which are missense mutation, 1 of which synonymous mutation, 1 nonsense mutation, 4 frameshift mutation, and 7 splicing site mutation. Among them, four mutations (p.T235K, c.1096-1G > A, p.A464A, and c.2660+1_2660+2insT) were novel mutations.ConclusionsWe found the preliminary evidence that the high-frequency mutation D486N in the Chinese population affected the expression of total and membrane-bound NCC protein and influenced the membrane localization of NCC protein. The findings of this study provides experimental evidence for genetic counseling, diagnosis, and treatment of Gitelman syndrome.
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Glucocorticoid-induced ocular hypertension(GIOH)is a condition characterized by elevated intraocular pressure caused by glucocorticoids. The long-term presence of GIOH may lead to optic nerve damage and visual field defects, eventually progressing to glucocorticoid-induced glaucoma(GIG), which can potentially cause blindness. Glucocorticoids primarily exert their biological effects by mediating glucocorticoid receptor(GR), while also involving factors such as transforming growth factor(TGF)-β, Wnt, and Rho in the formation of GIOH. In-depth exploration of the pathological changes and related molecular mechanisms of the trabecular meshwork in GIOH provides an important theoretical basis for understanding the pathogenesis and treatment of GIOH. Therefore, this article provides a review of the pathological changes and molecular mechanisms of the trabecular meshwork in GIOH, aiming to provide a theoretical basis for further research on the pathological mechanisms and treatment of GIOH.
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Fibrosis can occur in diverse tissue and organs and is the common outcome as multiple chronic diseases progress. It is characterized by over-activation of fibroblasts and excessive deposition of extracellular matrix. Targeting transforming growth factor-β （TGF-β）， a classical signaling molecule in fibrosis， is currently a routine strategy for drug therapy of this disease. The use of traditional Chinese medicine （TCM） in the treatment of fibrotic diseases has been supported by mature theories. The theories emphasize that the internally-accumulated pathogens and mixed deficiency-excess underlie the shared pathology of fibrotic diseases. Qi stagnation， blood stasis， phlegm turbidity， and mass accumulation are key pathological factors. "Yin suppression by Yang" is the core thought for treatment with TCM of the disease. Pharmacological investigations reveal the scientific nature of TCM in treating fibrotic diseases， namely multilevelled and multitargeted. In other words， it refers to networked regulation of signaling activities of fibrosis-related molecules such as TGF-β/Drosophila protein homolog （Smad）， phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）， Hedgehog， Wnt/β-catenin， and inflammatory cytokines， so as to inhibit fibroblast function and provide a promising insight into novel anti-fibrotic drug. This paper summarized the conventional understanding of fibrotic disease treatment with TCM and its mechanism of action by reviewing ancient literature and modern research reports， which offers an idea for follow-up research in this field.
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Diabetic retinopathy（DR） and coronary heart disease（CHD） are both major chronic vascular complications that seriously jeopardize the health of the population and often occur together in clinical practice， it is of great clinical value to actively explore the association between the two in the process of disease development and methods of prevention and treatment of modern medicine and traditional Chinese medicine（TCM）. According to TCM， the heart and eyes physiologically communicate with each other by taking Qi， blood and veins as bridges， blood stasis obstructing collaterals is the common TCM etiology of DR and CHD， whose mechanism involves inflammation， oxidative stress and endothelial dysfunction. Promoting blood circulation and removing blood stasis plays an important role in the same treatment for different diseases and prevention and treatment of comorbidities， possibly by inhibiting the expression of interleukin-1β（IL-1β）， endothelin-1（ET-1） and hypoxia inducible factor-1α/vascular endothelial growth factor（HIF-1α/VEGF）， regulating phosphatidylinositol 3-kinases/protein kinase B/mammalian target of rapamycin（PI3K/Akt/mTOR） pathway， initiating adenosine monophosphate（AMP）-activated protein kinase/silent information regulator 1（AMPK/SIRT1） and nuclear transcription factor erythroid 2-related factor 2/heme oxygenase-1（Nrf2/HO-1） signaling pathways， inhibiting Hippo/Yes-associated protein（Hippo/YAP） signaling pathway， inhibiting mitochondrial permeability transition pore and anti-platelet agglutination for treating DR and CHD， which provides a multi-component， multi-pathway and multi-target selection strategies and ideas for the prevention and treatment of DR and CHD by TCM from a biological perspective. Based on this， subsequent studies should focus on constructing clinically relevant comorbidity models， conducting multicenter prospective studies， and fully utilizing artificial intelligence technology to gain a deeper understanding of the relationship between the two diseases， so as to elucidate the mechanism of promoting blood circulation and removing blood stasis in preventing and treating panvascular diseases.
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Both parasitic diseases and cancers are disorders that seriously threaten human health. A strong correlation has been recently found between parasitic infections and cancers, and multiple species of parasites and their derived products have shown effective to suppress cancer development, progression and metastasis. Therefore, deciphering the interaction among parasites, cancers and hosts not only provides new insights into the development of cancer therapy, but also provides the basis for screening of parasites-derived active anticancer molecules. This review summarizes the latest advances in the anticancer activity of parasites and underlying mechanisms.
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As a widely used anti-tumor drug and anti-rheumatic drug in clinic, methotrexate (MTX) has many toxic and side effects, including gastrointestinal mucosa injury, central nervous system injury, liver and kidney function injury, etc. They often bring great trouble to the follow-up treatment of patients. The clarification of the mechanism of MTX toxicity to various organs has become the key to rescue the toxicity. The purpose of the article is to review the toxicity mechanism of MTX in various organs, so as to save the patients from the adverse reactions in clinical treatment.
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The senescence of bone marrow mesenchymal stem cells (BM-MSCs) will induce age-related bone tissue degeneration and chronic inflammation, and reduce its application effect for cell therapy. More and more active ingredients of traditional chinese medicine have been proved to intervene BM - MSCs senescence, playing an important role in bone diseases prevention and treatment, and improving the therapeutic effect of BM-MSCs. In this paper, the latest research progress on the molecular mechanism of traditional chinese medicine active ingredients interfering BM-MSCs senescence was summarized, in order to provide new direction and reference basis for senescence intervention research and clinical application improvement of BM-MSCs.
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ObjectiveThis study aimed at conducting retrospective analysis of the clinical symptoms and genetic mutations in 20 children with Gitelman syndrome treated at the Affiliated Children′s Hospital of Nanjing Medical University from August 2015 to November 2022 and also explored the molecular mechanism of the pathogenic high-frequency mutation D486N in the Chinese population.MethodsWe collected the clinical manifestations, growth and development status, laboratory examination results, and SLC12A3 gene variations of the patients. We distinguished the wild-type and mutant SLC12A3 genes overexpressed in human embryonic kidney 293T cells (HEK293T). We used protein immunoblotting to detect the expression level of NCC, and used immunofluorescence techniques to examine the subcellular localization of NCC. In addition, we investigated the impact of the high-frequency SLC12A3 gene mutation D486N on NCC protein expression and localization.ResultsIn the 20 patients with Gitelman syndrome, all of them had hypokalemia. We indemnified twenty-six SLC12A3 gene mutations, 13 of which are missense mutation, 1 of which synonymous mutation, 1 nonsense mutation, 4 frameshift mutation, and 7 splicing site mutation. Among them, four mutations (p.T235K, c.1096-1G > A, p.A464A, and c.2660+1_2660+2insT) were novel mutations.ConclusionsWe found the preliminary evidence that the high-frequency mutation D486N in the Chinese population affected the expression of total and membrane-bound NCC protein and influenced the membrane localization of NCC protein. The findings of this study provides experimental evidence for genetic counseling, diagnosis, and treatment of Gitelman syndrome.
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【Objective】 To study the relationship between ABO subtype, para-Bombay blood group and genotype, so as to explore the possible molecular mechanism of these two blood groups, and provide accurate genetic detection targets and theoretical basis for the accurate identification of ABO blood group. 【Methods】 First, the serology of 24 200 patients with blood type identification in the Ruijin Hospital from February to December in 2022 were analyzed, as well as 10 ambiguous ABO samples from other hospitals(3 were suspected ABO subtype and 7 were suspected para-Bombay blood group). Then ABO subtypes and para-Bombay blood groups were directly sequenced or post-clonal sequencing was performed to analyze ABO, FUT1 and FUT2 gene sequences. 【Results】 Among the 24 200 patients underwent blood type identification, 7 cases of ABO subtypes were detected. Among the 10 ambiguous samples sent by other hospitals, 2 of ABO subtypes, 1 of normal type A, and 7 of para-Bombay blood type were detected. In total, we identified blood types as follows: 1) 9 ABO subtypes: Ael(AEL.02/O.01.02), AelB(AEL.05/B.01), three of B3(2 of B3.03/O.01.01, 1 of B3.03/O.01.02), B(A)(BA.02/O.01.01), ABweak(A1.02/BW.07), Bweak(BW.31 /O.01.02), A2Bweak(A2.05 /BW.31); 2) 7 para-Bombay blood group: ABmh (FUT1*01N.13/FUT1*01N.13), 4 of Amh (3 of FUT1*01N.06/FUT1*01N.13, 1 of FUT1*01N.13/FUT1*01N.13); two of Bmh (FUT1*01N.06 /FUT1*01N.06, FUT1*01N.06/FUT1*01N.13), all of FUT2 of the 7 cases were FUT2*01/FUT2*01. 【Conclusion】 Clinical ABO blood group variant samples need to be identified in combination with serological and molecular biology to improve the accuracy of identification, thus providing a reference for safe blood transfusion, organ transplantation, and the prediction and prevention of fetal-maternal immune hemolytic disease.
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Pulmonary Arterial Hypertension （PAH） is a chronic progressive cardiopulmonary disease. The main pathological changes are vasoconstriction and pulmonary artery proliferative remodeling and right ventricular hypertrophy. Further exploration of the pathogenesis of PAH can reveal that its related pathways include vascular proliferation， vascular wall remodeling， oxidative stress， inflammatory response and gene regulation. Although great progress has been made in the treatment of PAH in recent years， the mortality rate is still high， current clinical treatments have not effectively improved the prognosis， and the disease has great impact on the physical， social， work and emotional aspects of patients. This article will review the latest research on the treatment of PAH， aiming to provide new clues for the clinical treatment of PAH.
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As a common clinical disease, fracture is often accompanied by pain, swelling, bleeding as well as other symptoms and has a high disability rate, even threatening life, seriously endangering patients' physical and psychological health and quality of life. Medical practitioners take many strategies for the treatment of fracture healing, including Traditional Chinese Medicine (TCM). In the early stage of fracture healing, the local fracture is often in a state of hypoxia, accompanied by the expression of hypoxia inducible factor-1α (HIF-1α), which is beneficial to wound healing. Through literature mining, we thought that hypoxia, HIF-1α and downstream factors affected the mechanism of fracture healing, as well as dominated this process. Therefore, we reviewed the local characteristics and related signaling pathways involved in the fracture healing process and summarized the intervention of TCM on these mechanisms, in order to inspirit the new strategy for fracture healing, as well as elaborate on the possible principles of TCM in treating fractures based on the HIF molecular mechanism.
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Icariin,which belongs to the class of flavonoids,is the main active ingredient of the traditional tonic Chinese herb Epimedii Folium.Modern studies have shown that icariin has a wide range of effects on the male reproductive system.It has various pharmacological activities such as regulating cell proliferation and apoptosis,antioxidants,promoting testosterone secretion,improving erectile function,inhibiting prostate cancer cell migration,invasion,and regulating cell cycle.It has research value and application prospects in the field of urology and assisted reproduction.Therefore,Icariin's pharmacological effects and molecular mechanisms on the male reproductive system are reviewed in this paper combined with literature visualization analysis.It is expected to provide a theoretical basis for the therapeutic value development and application of icariin in male reproductive health.