Histology and histopathology, Vol.41, Nº3, (2026)

Ir a Estadísticas

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http://hdl.handle.net/10201/202761

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    Cardiomyoprotective effect of Tanshinone IIA in diabetic cardiomyopathy achieved through enhancing PINK1-Parkin dependent mitophagy
    (2026) Chao Yu; Ping Li; Nannan Li; Ke Wu; Biología Celular e Histología
    This study aimed to explore the beneficial effects and underlying protection mechanism of Tanshinone IIA (TSIIA) in diabetic cardiomyopathy (DCM) from the perspectives of mitophagy and mitochondrial integrity. Here, we found that TSIIA significantly increased STZ-induced body weight (L-TSIIA, 299.5 vs. 276.3; H-TSIIA, 308.3 vs. 276.3) and reduced blood glucose concentration (H-TSIIA, 16.1 vs. 21.5). Meanwhile, TSIIA effectively restored the function and morphology of myocardial tissue in diabetes mellitus (DM) rats. Further, TSIIA has been confirmed to have a protective effect on the ultrastructure and function of myocardial mitochondria, which was achieved through activation of mitophagy, as evidenced by enhanced co-localization of LC3 and COX IV (H-TSIIA, 88188.0 vs. 14829.0). Mechanistically, TSIIA alleviated DCM via activation of the PINK1/Parkin axis, increasing PINK1 (H-TSIIA, 0.5 vs. 0.2), Parkin (H-TSIIA, 0.6 vs. 0.3), Beclin-1 (H-TSIIA, 0.6 vs. 0.2) and LC3II/I (H-TSIIA, 0.5 vs. 0.3) expression, as well as decreasing p62 (H-TSIIA, 1.4 vs. 3.6) expression. This study provided a novel insight into the protective effect of TSIIA in DCM and revealed, for the first time, that TSIIA could noticeably improve STZ-induced DCM by enhancing PINK1-Parkin dependent mitophagy.
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    Mechanism of the protective effect of 2,3,5,4'-Tetrahydroxy stilbene-2-O-β-D-glucoside on MPTP-induced Parkinson's disease mice
    (2026) Xiaolin Dong; Qingyun Li; Yanping Li; Furong Jin; Jingting Lu; Chengda Han; Lianbing Lin; Gang Wu1; Biología Celular e Histología
    Background and purpose. Parkinson's disease (PD) is a common neurodegenerative disorder with a complex pathogenesis. 2,3,5,4'-Tetrahydroxy stilbene-2-O-β-D-glucoside (TSG) is one of the main active components of Polygonum multiflorum Thunb., which has therapeutic effects in various neurodegenerative diseases. The aim of this study was to explore the influence of TSG on the PD process. Methods. The PD mouse model was constructed via the use of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The PD process was evaluated via behavioral tests, HE staining, immunohistochemistry, and immunofluorescence. The levels of related proteins and inflammatory factors were detected via western blotting and ELISA. The effect of TSG on the intestinal flora of MPTP-induced PD mice was evaluated through 16S rDNA sequencing. Results. TSG intervention can significantly alleviate motor dysfunction in PD mice, increase the number of TH-positive neurons in the substantia nigra, inhibit the accumulation of α-syn and glial cell activation, reduce the expression of the tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, iNOS, and COX2 proteins in the substantia nigra and colon, inhibit neuroinflamma-tion and intestinal inflammation, decrease the levels of LPS, LBP, TNF-α, IL-1β, and IL-6 in the serum, suppress systemic inflammation, reduce damage to the blood-brain barrier (BBB) and intestinal barrier in PD mice, and restore species diversity and abundance of the intestinal flora in PD mice to a certain extent. Conclusion. TSG can improve motor coordination ability, systemic and neuroinflammatory levels, BBB injury, intestinal barrier injury, and the intestinal flora composition of PD mice, suggesting that TSG has a protective effect on MPTP-induced PD mice.
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    Morphological changes in microglia in the mouse brain during postnatal development and obesity
    (2026) Chu Zhang; Ge Gao; Xiaonan Shao; YJing Kang; Xin Yan; Juntang Lin; Liang Qiao; Yang Li1; Biología Celular e Histología
    Microglia are innate immune cells in the central nervous system (CNS) and play critical roles in proper brain development and function. During postnatal development, microglia have a highly plastic morphology and change rapidly in response to the temporal brain environment. However, their dynamics and phenotypes during this period are still not fully elucidated. Here, we systematically elucidated microglial density and morphological changes during postnatal development as well as in pathological obese conditions. Our results demonstrated a spatiotemporal distribution of microglia in different brain regions associated with gradually increased microglial complexity during postnatal development. Moreover, microglia become reactive in most brain regions of obese mice, but their morphological diversity has a region-specific manner, with an obvious alteration in the hypothalamus. Overall, our data emphasized the morphological dynamics of microglia following developing time windows and provided the basic information for future investigations.
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    USP7 promotes follicular thyroid carcinoma progression and sorafenib resistance by activating NEK2/ATG5-mediated autophagy
    (2026) Jutao Zeng; Hong Cao; Jie Luo; Yingcheng Deng; Biología Celular e Histología
    Purpose. To investigate the role of ubiquitin-specific protease 7 (USP7) in thyroid cancer (TC) pathogenesis and sorafenib resistance. Methods. USP7 expression was compared in normal human thyroid cells and TC cells. The TC line with maximal differential USP7 expression was selected for further study. The functional interaction between USP7 and never in mitosis A (NIMA)-related kinase 2 (NEK2)/autophagy-related 5 (ATG5) was elucidated through a Pearson correlation coefficient analysis and co-immunoprecipitation assay. The half-inhibitory concentration (IC50) of sorafenib in resistant follicular thyroid (FTC) cells was determined following USP7 knockdown and ATG5 overexpression. Furthermore, the effects of USP7 knockdown and the autophagy inducer rapamycin (RAPA) on FTC cell function were assessed by colony formation and Transwell assays. The function of USP7 was validated in vivo using a xenograft mouse model, and tumor growth was assessed through gross examination and histopathological staining. Results. High USP7 expression promoted the proliferation, migration, and invasion of FTC cells and was positively correlated with NEK2 and ATG5 levels. USP7 enhanced NEK2 stability via deubiquitination. Knocking down USP7 downregulated ATG5, and this effect was reversed by NEK2 overexpression. USP7 inhibition reduced the IC50 of sorafenib in FTC cells, which was reversed by ATG5 overexpression. USP7 knockdown attenuated FTC cell proliferation, migration, and invasion while increasing the apoptosis rate, and these effects were reversed by RAPA treatment. Knocking down USP7 suppressed the growth of TC xenografts in vivo, improved tumor tissue differentiation, and reduced the percentage of Ki-67-positive cells. Conclusion. USP7 promoted the progression of FTC and induced sorafenib resistance by enhancing NEK2/ATG5-mediated autophagy. This study provides novel insights and potential therapeutic strategies for FTC treatment and overcoming drug resistance.
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    Suppressing SMURF1 to preserve GSTM2: An approach to reducing gastric cancer aggressiveness in vitro and in vivo
    (2026) Jingwu Li; Yuanting Liu; Weiwei Zuo; Guoming Ma; Biología Celular e Histología
    Background. Smad Ubiquitination Regulatory Factor-1 (SMURF1) is implicated in promoting gastric cancer progression by enhancing cell proliferation, migration, and invasion. This study aims to elucidate how SMURF1 drives gastric cancer aggressiveness, with a focus on its interaction with Glutathione S-transferase mu 2 (GSTM2). Methods. Bioinformatics analysis identified dysregulated SMURF1 and GSTM2 expression in stomach adenocarcinoma (STAD). The relation between GSTM2 and SMURF1 was predicted using Unibrowser. Functional assays, including cell counting kit-8, wound healing, and Transwell invasion, were conducted on gastric cancer cells to explore the effects of GSTM2 and/or SMURF1. The ubiquitination level of GSTM2 was measured using western blot and immuno-precipitation. In vivo tumorigenicity was assessed in a xenograft mouse model, alongside analysis of tumor growth and molecular markers of epithelial-mesenchymal transition (EMT). Results. SMURF1 was highly expressed and the GSTM2 level was significantly downregulated in STAD. GSTM2 silencing activated the viability, migration, and invasion of gastric cancer cells, and these cell functions were inhibited by GSTM2 overexpression, which was reversed by SMURF1 overexpression. SMURF1 was predicted to be an E3 ubiquitin ligase for GSTM2. SMURF1 overexpression or Cyclohexanecarboxamide (CHX) addition suppressed GSTM2 levels in gastric cancer cells. Silencing of SMURF1 restrained GSTM2 ubiquitination. In vivo, GSTM2 overexpression suppressed tumor growth and EMT markers, such as Vimentin, while elevating E-cadherin, which was offset by SMURF1 upregulation. Conclusion. This study reveals a novel oncogenic axis, where SMURF1 promotes gastric cancer progression by targeting GSTM2 for degradation. Inhibiting SMURF1 stabilizes GSTM2, leading to reduced cell proliferation, migration, and invasion both in vitro and in vivo.