Histology and histopathology最新文献

{"title":"Pachymic acid ameliorates polycystic ovary syndrome via inactivating Akt/ERK signaling.","authors":"Dongmei Ji, Chunhua Zhang, Fang Fang, Yuanyuan Yi","doi":"10.14670/HH-18-931","DOIUrl":"https://doi.org/10.14670/HH-18-931","url":null,"abstract":"<p><strong>Objective: </strong>Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder that adversely affects women's health and quality of life. Pachymic acid (PA), a bioactive ingredient from <i>Poria cocos</i> (Schw.) Wolf, has demonstrated protective effects against PCOS in a murine model. This study aims to investigate the underlying mechanism by which PA exerts protective effects against PCOS.</p><p><strong>Methods: </strong>Female Sprague-Dawley rats were treated with letrozole to induce PCOS. The ovarian granulosa cell line (KGN) was exposed to lipopolysaccharide (LPS) to mimic PCOS <i>in vitro</i>. Hematoxylin-eosin staining and TUNEL assay were used for ovarian histological analysis. The cell counting kit-8 assay was used to assess the viability of KGN cells. Flow cytometry was used for <i>in vitro</i> cell apoptosis analysis. Western blotting revealed molecular protein expression levels in rat ovaries and KGN cells.</p><p><strong>Results: </strong>PA attenuated LPS-induced lactate dehydrogenase release (p<0.01), reduced the cell apoptosis rate (p<0.001), Bax, and cleaved-caspase3 protein expression (p<0.001), and increased Bcl-2 protein expression (p<0.01) in KGN cells. PA attenuated letrozole-induced increases in testosterone (p<0.01), luteinizing hormone (p<0.01), and estradiol levels (p<0.05) and decreases in progesterone levels (p<0.05) in PCOS rats. PA promoted corpus luteum formation (p<0.001) and reduced the number of cystic follicles and cell apoptosis (p<0.001) in PCOS rats. PA blocked Akt and ERK signaling transduction in PCOS rats and KGN cells (p<0.001).</p><p><strong>Conclusion: </strong>PA protects against PCOS and attenuates cell apoptosis by inactivating Akt and ERK signaling.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18931"},"PeriodicalIF":2.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trophoblast-derived proteins and their effects on the pathogenesis of preeclampsia.","authors":"Ju Yang, Yanan Wang, Xueling Chen, Haifeng Zhang, Yunshan Xue, Haibin Chen","doi":"10.14670/HH-18-930","DOIUrl":"https://doi.org/10.14670/HH-18-930","url":null,"abstract":"<p><p>Trophoblast cells are crucial structural units of the placenta, responsible for maintaining its integrity and function. These cells synthesize and secrete specific proteins that play essential roles in placental vascularization, maternal and fetal immune tolerance, and other critical processes. An abnormal level of trophoblast-derived secreted proteins has been closely linked to pregnancy-related diseases. Preeclampsia, a severe complication of pregnancy characterized by <i>de-novo</i> development of hypertension and proteinuria after 20 weeks of gestation, poses significant health risks to both the mother and fetus. This article reviews several key trophoblast-derived proteins that are widely recognized for their roles in preeclampsia. The specific mechanisms of action and interconnections among these proteins in preeclampsia are discussed, along with novel insights into the underlying pathological mechanisms of this disease.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18930"},"PeriodicalIF":2.5,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periostin acts as an oncogene to promote laryngeal cancer progression by activating decorin.","authors":"Chao Wu, Bo Yang, Jiusheng Chu","doi":"10.14670/HH-18-804","DOIUrl":"10.14670/HH-18-804","url":null,"abstract":"<p><p>Laryngeal carcinoma (LC) is the second most common malignancy of the head and neck worldwide, with increasing incidence every year. However, the mechanism of its development is not completely clear. Periostin (POSTN) has been reported to be involved in various aspects of tumorigenesis. To determine the influence of POSTN on LC tumorigenesis, we first examined the expression of POSTN in tissues from patients with LC through immunohistochemistry, western blot, and qRT-PCR. Besides, we demonstrated that POSTN promoted LC cell migration, invasion, and proliferation <i>in vitro</i> by CCK-8, colony formation, and Transwell assays, and tumor growth <i>in vivo</i> by immunohistochemistry. Furthermore, the interaction between POSTN and decorin (DCN) was further verified by bioinformatics analysis and immunoprecipitation (IP), finding that POSTN promoted the malignant progression of LC by targeting DCN. Our findings support the idea that the level of POSTN expression and accumulation in tumors correlated with the malignancy degree of LC, suggesting that POSTN may play a potential role in improving laryngeal cancer treatment strategies.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"687-696"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Experimental murine models of interstitial cystitis/bladder pain syndrome: A review.","authors":"Tetsuichi Saito, Tomonori Minagawa, Naoki Yoshimura, Yi Luo, Yoshiyuki Akiyama","doi":"10.14670/HH-18-837","DOIUrl":"10.14670/HH-18-837","url":null,"abstract":"<p><p>Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic enigmatic disease of the urinary bladder characterized by persistent bladder/pelvic pain in conjunction with lower urinary tract symptoms. IC/BPS is categorized as either Hunner-type IC (HIC) or BPS based on the presence/absence of the Hunner lesion, a reddish mucosal lesion in the bladder. HIC and BPS present with similar symptoms, however, the etiologies are completely different. Recent evidence suggests that HIC is an immune-mediated inflammatory disease of the urinary bladder. In contrast, BPS, other forms of HIC lacking Hunner lesions, is a minimally inflamed condition comprising various clinical phenotypes. Based on this evidence, basic research into IC/BPS has shifted to target each subtype of IC/BPS. Today, experimental murine models of autoimmune cystitis are used for HIC research, whereas models related to neurophysiological and psychosocial dysfunctions have been developed for BPS research. This emerging concept of a subtype-tailored approach may contribute to a better understanding of the full picture of IC/BPS, thereby improving current clinical management strategies and the development of novel therapies.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"635-644"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular and immunohistochemical markers in appendiceal mucinous neoplasms: A systematic review and comparative analysis with ovarian mucinous neoplasms and colorectal adenocarcinoma.","authors":"Basel Elsayed, Amgad Mohamed Elshoeibi, Mohamed Elhadary, Abdullah M Al-Jubouri, Noof Al-Qahtani, Semir Vranic, Rafif Al-Saady","doi":"10.14670/HH-18-830","DOIUrl":"10.14670/HH-18-830","url":null,"abstract":"<p><strong>Introduction: </strong>Appendiceal mucinous neoplasms (AMNs) represent a rare and diagnostically challenging group of tumors. This systematic review aims to summarize the reported molecular and immunohistochemical markers (IHC) associated with AMNs and compare them with ovarian mucinous neoplasms (OMNs) and colorectal adenocarcinoma (CRC).</p><p><strong>Methods: </strong>A comprehensive search was performed in PubMed/MEDLINE/PMC, Scopus, Embase, and Web of Science databases to identify studies looking at IHC and molecular markers in AMNs. Chi-squared and Fisher's exact tests were utilized to compare the marker expression across different tumor types.</p><p><strong>Results: </strong>We identified 27 articles reporting several potential biomarkers for distinguishing between different subtypes of AMNs. Mutations in <i>KRAS</i>, <i>GNAS</i>, and <i>RNF43</i> emerged as notable biomarkers, with <i>KRAS</i> mutations being the most prevalent across all subtypes. Additionally, p53 IHC overexpression was associated with higher tumor grades. When comparing AMNs with OMNs, we observed a higher prevalence of CK20, CDX2, SATB2, and MUC2 IHC expression, as well as <i>KRAS</i> and <i>GNAS</i> mutations, in AMNs. Conversely, CK7 and PAX8 IHC expression were more prevalent in OMNs. Comparing AMNs with CRCs, we found a higher prevalence of TOPO1 and PTEN IHC expression, as well as <i>KRAS</i> and <i>GNAS</i> mutations, in AMNs. Conversely, nuclear β-catenin IHC expression, as well as <i>TP53</i>, <i>APC</i>, and <i>PIK3CA</i> mutations, were more prevalent in CRCs.</p><p><strong>Conclusion: </strong>This systematic review identified possible markers for distinguishing AMNs and differentiating between AMNs, OMNs, or CRCs.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"621-633"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142914683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does old-to-young kidney transplantation rejuvenate old donor kidneys?","authors":"Mayumi Takahashi-Kobayashi, Kunio Kawanishi, Joichi Usui, Satoshi Yamazaki, Surya V Seshan, Kunihiro Yamagata","doi":"10.14670/HH-18-829","DOIUrl":"10.14670/HH-18-829","url":null,"abstract":"<p><strong>Background: </strong>The number of older organ donors is increasing due to the aging population. Aged kidneys often face problems such as delayed graft function but previous murine experiments suggested the possibilities of rejuvenation, for example, in a parabiosis setting between old and young mice. To investigate kidney-graft rejuvenation, we compared an old-to-young (O-Y) patient transplantation group and a transplantation group with donors/recipients of approx. the same age (SA) with the renal senescence marker p16 in kidney biopsy samples at baseline and one year post-transplantation.</p><p><strong>Methods: </strong>We retrospectively analyzed our hospital's 32 cases of living-donor ABO-compatible transplants performed between 2013-2020. Both the baseline and one-year biopsy (n=9) or only the baseline biopsy (n=32) were analyzed. We divided the nine cases into an O-Y group (donors' median age 68 yrs, recipients 41, difference -27) and an SA group (donors' median age 53 yrs, recipients 51.5, difference -3.5). p16 was stained with the clones JC8 and E6H4 to determine the precise p16-positive rate.</p><p><strong>Results: </strong>The 32 baseline biopsies' p16-positive rate was weakly related to donor age, suggesting that the p16-positive rate can help evaluate kidney senescence. The (n=5) O-Y group's p16-positive rates were at baseline 0.08 and one year 0.12; the (n=4) SA group's rate was 0.03 at both baseline and one year.</p><p><strong>Conclusions: </strong>No kidney rejuvenation was observed, even when old donor kidneys went to young recipients.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"679-686"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142545179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ABRACL upregulated by transcription factor CBX4 promotes proliferation and migration and inhibits the apoptosis of gastric cancer cells.","authors":"Kai Guo, Xiao Gao","doi":"10.14670/HH-18-812","DOIUrl":"10.14670/HH-18-812","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) is a predominant health concern in many countries. Actin-binding Rho activating C-terminal-like (ABRACL) belongs to a new family of low molecular weight proteins and has been implicated in cancers. This study was implemented to elucidate the role and mechanism of ABRACL in GC.</p><p><strong>Methods: </strong>The mRNA and protein expression of ABRACL and CBX4 in human gastric epithelium cell line GES-1 and GC cell lines was assessed with RT-qPCR and western blot. The transfection efficacy of sh-ABRACL, oe-CBX4, and sh-CBX4 was examined with RT-qPCR and western blot. AGS cell proliferation, migration, and invasion were evaluated using CCK-8, colony formation assay, wound healing, and Transwell assays, respectively. With western blot analysis, flow cytometry, and caspase-3 assay kits, the expressions of MMP2 and MMP9, cell apoptosis, and caspase-3 activity were estimated. Western blot was adopted to estimate the contents of apoptosis-related proteins. Luciferase reporter and chromatin immunoprecipitation (ChIP) were applied to verify the interaction between ABRACL and CBX4.</p><p><strong>Results: </strong>The expression of ABRACL and CBX4 was increased in GC tissues and cells. After interfering with ABRACL, the proliferation, migration, and invasion of GC cells were inhibited while apoptosis was promoted. We also discovered that CBX4 could bind to ABRACL and transcriptionally regulate ABRACL expression in AGS cells. Rescue experiments revealed that CBX4 overexpression partially reversed the regulatory effects of ABRACL silencing on the proliferation, migration, invasion, and apoptosis of GC cells.</p><p><strong>Conclusion: </strong>Collectively, ABRACL transcriptionally upregulated by CBX4 promoted the malignant progression of GC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"721-732"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ameliorative effects of HGF-overexpressed exosomes derived from ADMSCs on oxidative stress in hepatic fibrosis.","authors":"Hanyu Zhou, Yanyan Wu, Junchao Xue, Liushenyan Yu","doi":"10.14670/HH-18-816","DOIUrl":"10.14670/HH-18-816","url":null,"abstract":"<p><strong>Background: </strong>Hepatic fibrosis, ultimately causing hepatic sclerosis, remains significant health concerns. Adipose-derived mesenchymal stem cell (ADMSC)-derived exosomes (Exo) exhibit amelioration of liver injury. Hepatocyte growth factor (HGF) regulates hepatocyte growthn. However, its involvement during hepatic fibrosis remains unclear.</p><p><strong>Methods: </strong>Isolation of ADMSCs and Exo, transfection of HGF overexpression, and activation of hepatic stellate cells (HSCs) by Angiotensin II (AngII) were conducted. Cells were randomized into HSC, AngII-HSC, ADMSCs-Exo, ADMSCs^blank-Exo, and ADMSCs^HGF-Exo, DPI, LY294002, and SB203580 groups. MTT for cell viability, cell migration, and flow cytometry for ROS were performed. BALB/c mice were treated with CCL4 for hepatic fibrosis models. The mice were randomized into Control, PBS, ADMSCs-Exo, ADMSCs^blank-Exo, and ADMSCs^HGF-Exo groups (n=6). HE, Sirius red, and Oil Red O staining, liver function indicators, and ELISA for oxidative stress were performed. ROS generation-related and PI3K/Akt/P38MAPK-related factors were detected by immunofluorescence, immunohistochemistry, and western blot.</p><p><strong>Results: </strong>After identification of ADMSC-Exo and transfection, AngII increased cell viability, migration, Collagen I (CoLI), α-smooth muscle actin (α-SMA), ROS, NADPH oxidase 4 (NOX4), PI3K, p-Akt, p-P38MAPK, ras-related C3 botulinum toxin substrate 1 (RAC1), p47^phox, and p22^phox expression. However, ADMSCs^HGF-Exo, DPI, LY294002, and SB203580 reversed the above effects. Moreover, ADMSCs^HGF-Exo inhibited pathological damage, fibrosis, lipid accumulation, ALT, AST, TBIL, CoLI, α-SMA, NOX4, MDA, PI3K, P-Akt, and P-P38MAPK expression, and increased ALB, SOD, GPx, CAT, GSH, Mn-SOD, Na⁺-K⁺-ATPase, and Ca²⁺-Mg²⁺-ATPase levels in hepatic fibrosis mice.</p><p><strong>Conclusion: </strong>ADMSCs^HGF-Exo attenuated hepatic fibrosis by inhibiting oxidative stress through activating the PI3K/Akt/P38MAPK pathway, providing valuable insights for potential treatment of liver fibrosis.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"757-772"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"G protein-gated inwardly rectifying K⁺ (GIRK/K_ir3) channels: Molecular, cellular, and subcellular diversity.","authors":"Alejandro Martín-Belmonte, Carolina Aguado, Rocio Alfaro-Ruíz, Rafael Luján","doi":"10.14670/HH-18-822","DOIUrl":"10.14670/HH-18-822","url":null,"abstract":"<p><p>G protein-gated inwardly rectifying K⁺ (GIRK/K_ir3) channels are mainly expressed in excitable cells such as neurons and atrial myocytes, where they can respond to a wide variety of neurotransmitters. Four GIRK subunits have been found in mammals (GIRK1-4) and act as downstream targets for various Gαi/o-linked G protein-coupled receptors (GPCRs). Activation of GIRK channels produces a postsynaptic efflux of potassium from the cell, responsible for hyperpolarization/inhibition of the neuron. A growing body of evidence suggests that dysregulation of GIRK signalling can lead to excessive or deficient neuronal excitability, which contributes to neurological diseases and disorders. Therefore, GIRK channels are proposed as new pharmacological targets. The function of GIRK channels in neurons is not only determined by their biophysical properties but also by their cellular and subcellular localization patterns and densities on the neuronal surface. GIRK channels can be located within several subcellular compartments, where they have many different functional implications. This subcellular localization changes dynamically along the neuronal surface in response to drug intake. Ongoing research is focusing on determining the proteins that form macromolecular complexes with GIRK channels and are responsible for fast and precise signalling under physiological conditions, and how their alteration is implicated in pathological conditions. In this review, the distinct regional, cellular, and subcellular distribution of GIRK channel subunits in the brain will be discussed in view of their possible functional and pathological implications.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"597-620"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin protects against sarcopenia in middle-aged mice.","authors":"Fei Fang, Ping Yu, Xiaoying Sun, Zhixing Shen, Fan Zhang, Jianwei Sun","doi":"10.14670/HH-18-814","DOIUrl":"10.14670/HH-18-814","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenia is a common age-related disease. Melatonin (MEL) is an age-related endocrine hormone, which displays a crucial role in resisting oxidative stress during aging. Importantly, the antioxidant properties of MEL can be mediated by mitochondria.</p><p><strong>Objective: </strong>Therefore, we wondered whether MEL could mitigate oxidative stress caused by mitochondria in sarcopenia.</p><p><strong>Methods: </strong>The middle-aged mice were administered 5 mg/kg/d and 10 mg/kg/d of MEL for 2 months. Young mice were used as the control group.</p><p><strong>Results: </strong>After treatment with MEL, the grip strength of the fore/hind limbs, running time, and distance were elevated, and the weights of the gastrocnemius (GA), tibialis anterior (TA), extensor digitorum longus (EDL), and soleus (SOL) were enhanced in middle-aged mice. Additionally, MEL was observed to alleviate histological damage and increase the cross-sectional area of muscle fibers in GA tissues of middle-aged mice. Furthermore, following MEL treatment, there was an increase in the percentage and size of normal mitochondria as well as mtDNA copy number but a reduction in the levels of malondialdehyde (MDA), protein carbonyl, and reactive oxygen species (ROS) in the GA tissues of middle-aged mice. At the molecular level, MEL repressed the levels of ATROGIN-1, muscle RING-finger protein-1 (MURF-1), and the ratio of p-P38/P38, but elevated the expression of cytochrome c oxidase subunit 4 (COX4), cystatin C (CYTC), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (TFAM), and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) in the GA tissues of middle-aged mice. Importantly, 10 mg/kg MEL was more efficacious in the treatment of sarcopenia than 5 mg/kg MEL.</p><p><strong>Conclusion: </strong>MEL attenuates sarcopenia in middle-aged mice, and the mechanism may relate to mitochondria-induced oxidative stress and the PGC-1α/TFAM pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"745-755"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}