Frontiers in Medicine
·
2025
·
IF 3
Ping Wang,Cunbo Yu,Yibing Li,Xiaoxiao Zhang,Xueli Yao,Yingjian Zhang
Introduction: This study aims to systematically explore the regulatory effects of ghrelin on hindlimb skeletal muscle function and gastrointestinal smooth muscle in mice. The objective is to elucidate the improvement effects of ghrelin on functional constipation through regulating skeletal muscle function and gastrointestinal motility, providing new theoretical support for the prevention and treatment of functional constipation.Methods: Dexamethasone-induced in vitro cell models and tail suspension-induced in vivo mouse models were employed to analyze the regulatory effect of ghrelin on the PI3K-Akt-mTORC1 signaling pathway. Additionally, a loperamide-induced constipation mouse model was used to evaluate the effects of ghrelin on fecal output, gastric motility, and smooth muscle activity. Experimental techniques included Western blotting, enzyme-linked immunosorbent assay (ELISA), histopathological staining, phenol red assay, and quantitative analyses of Ca2+ and ATP to comprehensively assess the impact of ghrelin on muscle atrophy and gastrointestinal function.Results: The results showed that, in vitro, ghrelin significantly upregulated the expression of p-AKT and reduced the levels of p-Foxo3a, effectively alleviating muscle atrophy. In vivo, the muscle condition of mice was improved and the expression of atrophy-related proteins (MAFbx and MuRF1) decreased, promoting the functional recovery of hindlimb muscles. In constipated mice, ghrelin increased fecal water content and defecation frequency, and accelerated gastric emptying, findings consistent with elevated ghrelin levels in serum and tissue. Moreover, ghrelin promoted calcium ion influx and ATP production in gastric smooth muscle cells, thereby enhancing gastrointestinal motility.Discussion: In conclusion, ghrelin effectively alleviates muscle atrophy by activating the PI3K-Akt-mTORC1 signaling pathway, and improves gastrointestinal motility by enhancing smooth muscle activity. These findings highlight ghrelin’s potential as an effective therapy for functional constipation.
研究领域:
生理学
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药理学
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胃肠病学
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内分泌学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
GENERAL AND COMPARATIVE ENDOCRINOLOGY
·
2018
·
IF 2.564
Xixi Song,Hongchao Jiao,Jingpeng Zhao,Xiaojuan Wang,Hai Lin
Ghrelin is one of the most important appetite regulating peptides, involved in the regulation of energy homeostasis. The role of ghrelin on the appetite and fat metabolism in chickens is different from that of ghrelin in mammals. Glucocorticoids and insulin are important hormones and work differently in energy regulation of body. In this study, the effects of dexamethasone (DEX, 2.0 mg/kg BW), subcutaneous insulin injection (40 µg/kg BW), and glucose load on ghrelin secretion and expression were determined in broilers. DEX treatment increased circulating ghrelin concentration in broiler fed with either a low-energy diet (11.05 MJ/kg of metabolizable energy) or a high-energy diet (14.44 MJ/kg of metabolizable energy). The expression levels of ghrelin were increased while both ghrelin and its receptor GHS-R1a expression levels were stimulated by DEX. A single subcutaneous insulin injection (40 µg/kg BW) or oral glucose infusion (2 g/kg BW) rise circulating ghrelin level. Ghrelin expression in the proventriculus was increased by insulin treatment but unchanged by glucose load. DEX had no detectable influence on ghrelin and GHS-R1a expression in the hypohtalamus, whereas insulin suppressed their expression. In conclusion, both insulin and glucocorticoid stimulate ghrelin secretion in chickens, in contrast to mammals. Glucocorticoids evoke peripheral ghrelin/GHS-R1a system while insulin increases peripheral ghrelin expression and suppress the activation of central ghrelin/GHS-R1a system. The result suggests that ghrelin involved in the modulating network of energy homeostasis in concert with glucocorticoids and insulin.
研究领域:
动物科学
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内分泌学
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营养学
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产品关联
DOI
PubMed
高影响因子
FASEB JOURNAL
·
2024
·Vol. 38
·期 11
·e23681
·
IF 4.4
Shi-shi Liao,Le-le Zhang,Yi-guo Zhang,Jie Luo,Tulanisa Kadier,Ke Ding,Rong Chen,Qing-tao Meng
Ischemia–reperfusion (IR) injury is primarily characterized by the restoration of blood flow perfusion and oxygen supply to ischemic tissue and organs, but it paradoxically leads to tissue injury aggravation. IR injury is a challenging pathophysiological process that is difficult to avoid clinically and frequently occurs during organ transplantation, surgery, shock resuscitation, and other processes. The major causes of IR injury include increased levels of free radicals, calcium overload, oxidative stress, and excessive inflammatory response. Ghrelin is a newly discovered brain-intestinal peptide with anti-inflammatory and antiapoptotic effects that improve blood supply. The role and mechanism of ghrelin in intestinal ischemia–reperfusion (IIR) injury remain unclear. We hypothesized that ghrelin could attenuate IIR-induced oxidative stress and apoptosis. To investigate this, we established IIR by using a non-invasive arterial clip to clamp the root of the superior mesenteric artery (SMA) in mice. Ghrelin was injected intraperitoneally at a dose of 50 μg/kg 20 min before IIR surgery, and [D-Lys3]-GHRP-6 was injected intraperitoneally at a dose of 12 nmol/kg 20 min before ghrelin injection. We mimicked the IIR process with hypoxia-reoxygenation (HR) in Caco-2 cells, which are similar to intestinal epithelial cells in structure and biochemistry. Our results showed that ghrelin inhibited IIR/HR-induced oxidative stress and apoptosis by activating GHSR-1α. Moreover, it was found that ghrelin activated the GHSR-1α/Sirt1/FOXO1 signaling pathway. We further inhibited Sirt1 and found that Sirt1 was critical for ghrelin-mediated mitigation of IIR/HR injury. Overall, our data suggest that pretreatment with ghrelin reduces oxidative stress and apoptosis to attenuate IIR/HR injury by binding with GHSR-1α to further activate Sirt1.
研究领域:
药理学
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病理生理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
MOLECULAR NEUROBIOLOGY
·
2026
·Vol. 63
·期 1
·650
·
IF 5.5
Guo Yaoxue,Wang Xueyan,Zhang Lixiang,Liu Xing,Lu Pu,Liang Furu,Wu Jing,Zhao Junli,Hai Yan
Alzheimer’s disease (AD) is associated with mitochondrial dysfunction and impaired energy metabolism in astrocytes. Although ghrelin is known to exert neuroprotective effects, the mechanisms through which it modulates astrocyte bioenergetics under AD-like conditions remain incompletely defined. In primary astrocytes treated with Aβ 25-35 oligomers, ghrelin attenuated mitochondrial damage, reducing ROS and enhancing mitochondrial membrane potential (ΔΨm) and respiratory complex activities. Glycolytic function was partially restored, as evidenced by upregulation of key enzymes, increased glucose uptake, lactate release, and NAD + /NADH ratio. Ghrelin inhibited autophagosome formation while enhancing mitophagy (increased LC3II/I and Parkin) and suppressed inflammation. In co-culture models, these metabolic improvements enhanced astrocytic support for neurons, reducing apoptosis and promoting neurite growth, an effect abolished by the glycolytic inhibitor 2-DG. Mechanistically, ghrelin upregulated uncoupling protein 2 (UCP2), which inhibited forkhead box protein O1 (FOXO1) nuclear translocation. In Aβ 25-35 -injected mice with UCP2 or FOXO1 modulation, ghrelin improved cognitive performance and reduced pathology, effects that were negated by UCP2 knockdown and partially rescued by FOXO1 knockdown. In conclusion, ghrelin ameliorates Aβ-induced astrocyte dysfunction involving the UCP2-FOXO1 pathway, partially restoring mitochondrial integrity, glycolytic metabolism, and neurotrophic support, suggesting its therapeutic potential.
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF THROMBOSIS AND THROMBOLYSIS
·
2024
·
IF 2.3
He Chengjian,Song Xiaojing,Zhu Zigui,Xiao Yan,Chen Jiacheng,Yao Hongyi,Xie Rongjun
Ghrelin exerts widespread effects in several diseases, but its role and mechanism in Acute Traumatic Coagulopathy (ATC) are largely unknown. The effect of ghrelin on cell proliferation was examined using three assays: 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), Lactate Dehydrogenase (LDH), and flow cytometry. The barrier function of the endothelial cells was evaluated using the Trans-Endothelial Electrical Resistance (TEER) and the endothelial permeability assay. An ATC mouse model was established to evaluate the in vivo effects of ghrelin. The Ras homolog family member A (RhoA) overexpression plasmid or adenovirus was used to examine the molecular mechanism of ghrelin. Ghrelin enhanced Human Umbilical Vein Endothelial Cells (HUVEC) proliferation and endothelial cell barrier function and inhibited HUVEC permeability damage in vitro. Additionally, ghrelin decreased the activated Partial Thromboplastin Time (aPTT) and Prothrombin Time (PT) in mice blood samples in the ATC mouse model. Ghrelin also improved the pathological alterations in postcava. Mechanistically, ghrelin acts through the RhoA/ Rho-associated Coiled-coil Containing Kinases (ROCK)/ Myosin Light Chain 2 (MLC2) pathway. Furthermore, the protective effects of ghrelin, both in vitro and in vivo, were reversed by RhoA overexpression. Our findings demonstrate that ghrelin may reduce vascular endothelial cell damage and endothelial barrier dysfunction by blocking the RhoA pathway, suggesting that ghrelin may serve as a potential therapeutic target for ATC treatment. Graphical Abstract We explored the effects of ghrelin on coagulopathy and vascular endothelial injury in vivo by establishing an ATC mouse model, and investigated the effects of ghrelin on LPS-induced HUVECs cell damage in vitro. The RhoA overexpression plasmid or adenovirus was used to examine the molecular mechanism. Abbreviations : ATC =acute traumatic coagulopathy; HUVECs =Human Umbilical Vein Endothelial Cells; LPS =lipopolysaccharide; RhoA =The Ras homolog family member A; aPTT =activated partial thromboplastin time; PT =prothrombin time; TEER =trans-endothelial electrical resistance
研究领域:
血液学
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血管生物学
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药理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
IN VIVO
·
2024
·Vol. 38
·期 3
·1133-1142
·
IF 1.8
LONGJIE XU,LILI HOU,CHUN CAO,XIAOHUA LI
Background/Aim: Cancer-induced bone pain (CIBP) is one of the most common symptoms of bone metastasis of tumor cells. The hypothalamus may play a pivotal role in the regulation of CIBP. However, little is known about the exact mechanisms. Materials and Methods: First, we established a CIBP model to explore the relationship among hypothalamic ghrelin, NPY and CIBP. Then, we exogenously administered NPY and NPY receptor antagonists to investigate whether hypothalamic NPY exerted an antinociceptive effect through binding to NPY receptors. Finally, we exogenously administered ghrelin to investigate whether ghrelin alleviated CIBP by inducing the production of hypothalamic NPY through the AMPK-mTOR pathway. Body weight, food intake and behavioral indicators of CIBP were measured every 3 days. Hypothalamic ghrelin, NPY and the AMPK-mTOR pathway were also measured. Results: The expression of hypothalamic ghrelin and NPY was simultaneously decreased in cancer-bearing rats, which was accompanied by CIBP. Intracerebroventricular (i.c.v.) administration of NPY significantly alleviated CIBP in the short term. The antinociceptive effect of NPY was reversed with the i.c.v. administration of the Y1R and Y2R antagonists. The administration of ghrelin activated the AMPK-mTOR pathway and induced hypothalamic NPY production to alleviate CIBP. This effect of ghrelin on NPY and antinociception was reversed with the administration of a GHS-R1α antagonist. Conclusion: Ghrelin could induce the production of hypothalamic NPY through the AMPK-mTOR pathway to alleviate CIBP, which can provide a novel therapeutic mechanism for CIBP.
研究领域:
神经科学
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疼痛研究
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肿瘤学
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药理学
✓ 已验证
DOI
PubMed
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2025
·
IF 3.4
Yanan Xia,Lihua Feng,Yuzhi Lan,Xiangxiang Chen,Xiaomin Tang,Hengyi Xu,Yang Liu
Children's daily exposure to titanium dioxide nanoparticles (TiO₂ NPs) poses significant risks to the developing testes, yet few studies have examined their impact on young testicular growth. Given ghrelin's established antioxidant and testis-protective effects in animal models, we hypothesized that it could mitigate TiO₂ NPs–induced damage. In this first systematic investigation of young testicular responses, three-week-old male rats received oral gavage of TiO₂ NPs (100, 200, or 400 mg/kg), followed 30 min later by intraperitoneal ghrelin (50 mg/kg) for four weeks. Exposure to TiO₂ NPs disrupted seminiferous tubule architecture and reduced serum levels of key developmental and sex hormones, including IGF-1, FSH, LH, and testosterone. Mechanistically, TiO₂ NPs activated the ROS/AMPK/mTOR signaling pathway, resulting in a marked reduction of SOD, CAT, and GSH activities and the induction of oxidative imbalance, while simultaneously upregulating the autophagy protein ULK1 and autophagy-related genes to trigger excessive autophagy, ultimately compromising testicular architecture and function. We further assessed ghrelin's protective efficacy against TiO₂ NPs-induced reproductive injury in young rats, demonstrating that ghrelin inhibited the ROS/AMPK/mTOR signaling pathway, attenuated oxidative stress, and suppressed excessive autophagy, thereby mitigating testicular injury. These findings represent the first evidence of the developing testicular heightened vulnerability to TiO₂ NPs toxicity and underscore ghrelin's potential as a novel protective intervention. Our study provides new insights into the reproductive toxicology of engineered nanoparticles and supports targeted strategies to safeguard pediatric reproductive health.
研究领域:
毒理学
·
生殖健康
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纳米生物学
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产品关联
DOI
PubMed
高影响因子
AGING CELL
·
2026
·Vol. 25
·期 10
·e70732
·
IF 7.7
Lixing Zhou,Ying Cheng,Wanyu Zhao,Xuelian Sun,Fengjuan Hu,Meiling Ge,Yan Zhang,Gongchang Zhang,Birong Dong,Xiaolei Liu
Cognitive impairment (CI) associated with aging and immunosenescence is linked to metabolic alterations. Microglial senescence and dysregulated autophagy have been implicated as major contributors to this process, but the underlying metabolic regulators remain unclear. This study aimed to identify key metabolic regulators of CI and elucidate their underlying mechanisms. Human cohort analyses, older and D‐galactose (D‐gal)‐induced mouse models, and microglial cell models were integrated to investigate the metabolic regulation of CI. Clinical analyses identified ghrelin as the factor most strongly associated with CI. Older and D‐gal mice exhibited CI, microglial senescence, enhanced inflammation, and elevated ghrelin. Ghrelin treatment improved cognitive function, attenuated microglial senescence, and suppressed inflammation, whereas high‐dose ghrelin induced growth hormone secretagogue receptor (GHSR) desensitization. Sex hormone‐binding globulin (SHBG) showed mainly cytoplasmic localization, was identified as a potential mediator of ghrelin signaling in microglia, and its expression was downregulated following ghrelin treatment. Transcriptomic profiling revealed significant enrichment of autophagy‐related pathways in ghrelin‐treated microglia. Ghrelin altered autophagy‐related markers, as indicated by increased Beclin1 and LC3 and decreased p62. SHBG overexpression or JNK1 inhibition attenuated the ghrelin‐induced alterations in autophagy‐related markers and anti‐senescent effects, whereas Beclin1 overexpression partially rescued these inhibitory effects caused by SHBG overexpression. In conclusion, ghrelin alleviated aging‐related CI, with mechanistic evidence indicating that the modulation of microglial autophagy‐related mechanisms through the SHBG/JNK1/Beclin1 axis may contribute to its protective effects, thereby providing a potential therapeutic strategy for aging‐related CI. This study found that aging‐related cognitive impairment is accompanied by hippocampal microglial senescence. Ghrelin suppresses microglial senescence by promoting autophagy through the SHBG/JNK1/Beclin1 axis, thereby alleviating aging‐related cognitive impairment. The graphical abstract was drawn using the Figdraw.
✓ 已验证
DOI
PubMed
高影响因子
BIOCHIMIE
·
2024
·
IF 3.3
Bing Wu,Songxia Cheng,Fuyan Liu,Jia Wei,Yongling Liu,Teng Qian,Jiali Ding,Biao Xu,Jie Wei
It is widely recognized that developing bi- or multifunctional opioid compounds could offer a valuable approach to pain management with fewer side effects compared to single-target compounds. In this study, we designed and characterized two novel chimeric peptides, EM-1-DLS and EM-2-DLS, incorporating endomorphins (EMs) and the ghrelin receptor antagonist [D-Lys3]-GHRP-6 (DLS). Functional assays demonstrated that EM-1-DLS and EM-2-DLS acted as κ-opioid receptor (κ-OR)-preferring agonists, weak μ-opioid receptors (μ-OR) and ghrelin receptor (GHSR) agonists. Upon intracerebroventricular (i.c.v.) administration in mice, both EM-1-DLS and EM-2-DLS exhibited dose- and time-dependent antinociceptive effects in the tail withdrawal test. EM-1-DLS demonstrated the highest antinociceptive potency among the peptides, with an ED 50 approximately 8-fold greater than EM-1, while EM-2-DLS showed comparable effects to EM-2. The antinociceptive actions of EM-1-DLS involved activation of GHS-R1α, μ-OR, and κ-OR, whereas EM-2-DLS acted via GHS-R1α, δ-OR, and κ-OR pathways. Additionally, acute antinociceptive tolerance was investigated, revealing that EM-1-DLS induced a tolerance ratio of 2.33-fold, significantly lower than the 5.19-fold ratio induced by EM-1. Cross-tolerance ratios between the chimeric peptides and EMs ranged from 0.92 to 1.76, indicating reduced tolerance compared to EMs alone. These findings highlight the potential of these chimeric peptides to mitigate pain with diminished tolerance development, suggesting a promising strategy for the development of new analgesic therapies with improved safety profiles.
研究领域:
药理学
·
疼痛管理
·
神经科学
✓ 已验证
DOI
高影响因子
Molecular Medicine Reports
·
2023
·Vol. 28
·期 3
·1-14
·
IF 3.4
Gui-Bo Liu,Yong-Xia Cheng,Hua-Min Li,Yong Liu,Li-Xin Sun,Qi Wu,Shang-Fu Guo,Ting-Ting Li,Chuan-Ling Dong,Ge Sun
Adipose tissue‑derived mesenchymal stem cells (ADMSCs) differentiate into cardiomyocytes and may be an ideal cell source for myocardial regenerative medicine. Ghrelin is a gastric‑secreted peptide hormone involved in the multilineage differentiation of MSCs. To the best of our knowledge, however, the role and potential downstream regulatory mechanism of ghrelin in cardiomyocyte differentiation of ADMSCs is still unknown. The mRNA and protein levels were measured by reverse transcription‑quantitative PCR and western blotting. Immunofluorescence staining was used to show the expression and cellular localization of cardiomyocyte markers and β‑catenin. RNA sequencing was used to explore the differentially expressed genes (DEGs) that regulated by ghrelin. The present study found that ghrelin promoted cardiomyocyte differentiation of ADMSCs in a concentration‑dependent manner, as shown by increased levels of cardiomyocyte markers GATA binding protein 4, α‑myosin heavy chain (α‑MHC), ISL LIM homeobox 1, NK2 homeobox 5 and troponin T2, cardiac type. Ghrelin increased β‑catenin accumulation in nucleus and decreased the protein expression of secreted frizzled‑related protein 4 (SFRP4), an inhibitor of Wnt signaling. RNA sequencing was used to determine the DEGs regulated by ghrelin. Functional enrichment showed that DEGs were more enriched in cardiomyocyte differentiation‑associated terms and Wnt pathways. Dead‑box helicase 17 (DDX17), an upregulated DEG, showed enhanced mRNA and protein expression levels following ghrelin addition. Overexpression of DDX17 promoted protein expression of cardiac‑specific markers and β‑catenin and enhanced the fluorescence intensity of α‑MHC and β‑catenin. DDX17 upregulation inhibited protein expression of SFRP4. Rescue assay confirmed that the addition of SFRP4 partially reversed ghrelin‑enhanced protein levels of cardiac‑specific markers and the fluorescence intensity of α‑MHC. In conclusion, ghrelin promoted cardiomyocyte differentiation of ADMSCs by DDX17‑mediated regulation of the SFRP4/Wnt/β‑catenin axis.
研究领域:
干细胞生物学
·
心血管研究
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分子生物学
·
再生医学
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产品关联
DOI
PubMed
高影响因子
Fishes
·
2023
·Vol. 8
·期 3
·170
·
IF 2.3
Lei Zhang,Peng Shi,Lin Zhang,Yajun Wang,Jilin Xu,Xiaojun Yan,Kai Liao
Ghrelin, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY) are potent hormones mediating food intake according to the nutritional status in fish. However, limited information is available on these genes and their expression in response to nutrition in silver pomfret (Pampus argenteus). A comparison analysis revealed thatghrelinand GLP-1 were relatively conserved in marine fish. PYYa and PYYb shared a low identity and were clustered to different PYY branches.Ghrelin,pyya, andpyybmRNAs were highly expressed in the brain, whileglp-1was highly expressed in the gills and liver. TheghrelinmRNA expression was relatively high an hour post-feeding and decreased after 3 to 72 h of fasting. Theglp-1mRNA expression was increased after 6 to 24 h of fasting. ThepyyamRNA expression was increased after 72 h of fasting, while thepyybexpression remained stable during fasting. The diet with 14% lipid promoted the expressions ofglp-1,pyya, andpyyb, but inhibited theghrelinexpression. Theghrelinexpression in the intestine was increased after palmitic acid, oleic acid (OA), linoleic acid (LA), α-linolenic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) incubation. OA decreased the expression ofglp-1and increased the expression ofpyya. The expression ofpyybwas downregulated by LA, DHA, and EPA. These results suggest the importance ofghrelin,glp-1, andpyyin coordinating food intake in response to fasting, dietary lipid concentration, and fatty acids in silver pomfret.Keywords:ghrelin;glp-1;pyy;fasting;lipid content;fatty acids;silver pomfretKey Contribution:This study provides insight into howghrelin,glp-1, andpyyrespond to fasting, dietary lipid concentration, and fatty acids in silver pomfret.
研究领域:
海洋生物学
·
分子生物学
·
营养学
✓ 已验证
产品关联
DOI
高影响因子
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
·
2021
·
IF 4.698
Xixi Song,Minghui Wang,Hongchao Jiao,Jingpeng Zhao,Xiaojuan Wang,Hai Lin
Ghrelin, classically known as a central appetite-stimulating hormone, has recently been recognized to play an important role in peripheral tissue energy metabolism. In chicken, contrary to mammal, ghrelin acts as an anorexia signal, increased by fasting and further elevated after refed. In the present study, the effect of ghrelin on glucose/lipid utilization by peripheral tissues was investigated. Injection of exogenous acyl ghrelin reduced plasma triglyceride and glucose levels of chickens at both fasting and fed status. In the in vitro cultured chicken primary hepatocytes, adipocytes, and myoblasts, ghrelin suppressed glucose uptake , stimulated fatty acids uptake and oxidation , and decreased TG content. In hepatocyte, ghrelin increased the activities of LPL and HL, and upregulated the expression levels of gene ACC , CPT1 , and PPARα . Ghrelin treatment markedly increased the protein level of p-ACC, PPARγ, PGC1α, and CPT1 in hepatocytes, adipocytes and myoblasts. Inhibition of AMPK activity by Compound C had no influence on glucose uptake by hepatocyte, adipocyte, and myoblast, but further amplified the stimulated fatty acid uptake of adipocyte by ghrelin. The present result demonstrates that ghrelin facilitates the uptake and oxidation of fatty acid and cut down the utilization of glucose by the liver, muscle, and adipose tissues. The result suggests that ghrelin functions as a signal of fatty acid oxidation. The study provides a vital framework for understanding the intrinsic role of ghrelin as a crucial factor in the concerted regulation of metabolic substrate of hepatocytes, adipocytes, and myoblasts.
研究领域:
内分泌学
·
代谢
·
动物生理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）