Acta Universitatis Medicinalis Anhui

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Weng Jianping

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ISSN 1000 - 1492

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Current situation and future of robotic telesurgery

Yue Jiabin；Tai Sheng； Liang Chaozhao

DOI: 10.19405/j.cnki.issn1000-1492.2026.01.002

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Research progress of urea-containing PET tracers targeting prostate specific membrane antigen

Zhu Hong1，2，Wang Hui2，Si Hongwei2，Zhang Dan2，Chen Dengyun2，Dai Pengfei1，2

DOI: 10.19405/j.cnki.issn1000-1492.2026.02.025

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Analysis of follicular helper T cell percentage and expression levels of functionally related cytokines in a mouse model of incomplete embryo implantation disorders

Wang Peng1，Gong Xiaoyun1，Zhang Manli1，Zhang Yunian1，La Xiaolin1，2，3，4

DOI: 10.19405/j.cnki.issn1000-1492.2026.01.007

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abstract:
To detect the proportion of splenic follicular helper T（Tfh）cells and their functionally re- lated cytokine expression levels in the incomplete embryo implantation disorder（EID）model mice，and to explore the immunological mechanism of Tfh in infertility caused by embryo implantation disorder. Methods Sixteen fe- male Kunming mice were randomly divided into two groups，with eight mice in each group. On day 4 of pregnancy， an incomplete EID mouse model was established by oral gavage of mifepristone suspension，while an equal volume of saline was administered to the control group. On day 8 of pregnancy，the mice were euthanized. Flow cytometry was used to detect the levels of Tfh cells in the spleen lymphocytes of both incomplete EID mice and normal control mice. qRT-PCR was performed to measure the mRNA levels of B-cell lymphoma 6（Bcl-6）and C-X-C chemokine receptor type 5 protein（CXCR5）in the spleen lymphocytes of both groups. Western blot was employed to assess the protein expression levels of Bcl-6 and CXCR5 in the spleen lymphocytes of both groups. Serum levels of inter- leukin-4（IL-4）， IL-6，and IL-21 were measured by ELISA. Immunohistochemistry（IHC）was used to observe the expression levels of progesterone receptor（PR），Bcl-6，and CXCR5 proteins in the uterine endometrial tissue of mice in both groups. Results Incomplete-type EID mice had a reduced number of embryo implantation points and reduced endometrial PR expression. Flow assay results showed that the proportion of CD4+CXCR5+Tfh cells in splenic lymphocytes of incomplete-type EID mice was significantly higher than that of normal controls（P<0. 05）.Compared with the normal control group，Bcl-6 and CXCR5 mRNA levels and protein levels were elevated in splenic lymphocytes of incomplete EID mice，with statistically significant differences（P<0. 05）；serum IL-4，IL- 6，and IL-21 levels were elevated in incomplete EID mice，and Bcl-6 and CXCR5 proteins in the endometrium were significantly elevated（P<0. 05）. Conclusion The increase of Tfh cells and their associated cytokines Bcl-6 and CXCR5 is associated with the development of incomplete EID，and may be involved in the development of fe- male immune infertility.

Analysis of the incidence and mortality trends of type 2 diabetic nephropathy in China from 1990 to 2021

Dou Xuewei，Cui Wenfei，Niu Ling，Yin Binglei，Wang Jinjin

DOI: 10.19405/j.cnki.issn1000-1492.2026.01.027

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NGR1 modulates mitophagy in human cardiomyocytes via the Pink1/Parkin pathway after hypoxia/reoxygenation

Xiong Xiaoman1，Wu Huan1，Lu Shanglin2，Wang Yong1，Zheng Yuhua1，Xiang Yi1，Zhou Haiyan2，Liu Xingde1

DOI: 10.19405/j.cnki.issn1000-1492.2026.01.009

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abstract:
To investigate the mechanism by which Notoginsenoside R1（NGR1）ameliorates hypoxia/reoxygenation（H/R）-induced injury in AC16 human cardiomyocyte cell lines through the regulation of mitophagy. Methods Common genes linked to hypoxia/reoxygenation injury and mitophagy were identified by intersecting data from GeneCards and MitoCarta databases. AC16 cell viability was assessed via CCK-8 assay under varying NGR1 concentrations（0，6. 25，12. 5，25，50，100，200，300，400，500 μmol/L）. AC16 cells were divided into the following groups：control group（Control），model group（H/R），and treatment groups（H/R + NGR1 at 100， 200，and 300 μmol/L）. Mitochondrial membrane potential ( ΔΨm）was measured using 5，5'，6，6'-tetrachloro-1， 1'，3，3'-tetraethylbenzimidazolylcarbocyanine iodide（JC-1）staining. Transcriptional levels of mitophagy-related genes（Parkin，Pink1，P62）were quantified by reverse transcription-quantitative PCR（RT-qPCR）. Protein ex- pression of mitophagy-related markers（Parkin，Pink1，P62，and LC3BII）was evaluated via Western blot analy- sis. Mitochondrial ultrastructure was visualized by transmission electron microscopy（TEM）. Results Compared to the control group，cell viability in the H/R group significantly decreased（P<0. 01）. Treatment with NGR1 at concentrations above 100 μmol/L significantly enhanced the cell viability of AC16 cells compared to the H/R group （P<0. 01）. H/R induced a significant decrease in mitochondrial membrane potential（P<0. 01）， which was re- stored by NGR1 treatment（P<0. 01）. The mRNA levels of Parkin，Pink1，and P62 in the H/R group were upregu- lated compared to the control group（ P<0. 05）， while NGR1 intervention downregulated their expression（ P< 0. 05）. Protein expression levels of Parkin，Pink1，and LC3BII in the H/R group significantly increased，while P62 expression decreased compared to the control group（P<0. 01）. In contrast，different doses of NGR1 treatment significantly reduced the expression of Parkin，Pink1，and LC3BII while increasing P62 expression（P<0. 05）. TEM revealed that the mitochondrial structure in the H/R group was severely disrupted，with fragmented and disor- ganized cristae，which was alleviated by NGR1. Conclusion NGR1 ameliorates H/R-induced AC16 cell injury， and its mechanism may be associated with modulating the Pink1/Parkin pathway to suppress excessive mitophagy.

The role of S100A2 in the progression of colorectal cancer

Huo Yishan1，Duan Xiangbing1，Xu Xiaohui1，Li Tao2，Ma Xiumin1

DOI: 10.19405/j.cnki.issn1000-1492.2026.01.020

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abstract:
To investigate the role of calcium-binding protein S100A2 in colorectal cancer（CRC）pro- gression and its association with fructose metabolism in CRC cells. Methods Differential expression of S100A2 be- tween CRC patients and healthy individuals was analyzed using the GEPIA2 tumor database. Western blot and qRT-PCR were performed to compare S100A2 expression levels in CRC cell lines（HCT116，SW480，Caco-2）and normal human colonic epithelial cells（NCM460）. Immunohistochemical staining was conducted to assess S100A2 expression in CRC tissues and adjacent non-tumor tissues. S100A2-knockdown stable CRC cell lines and negative control cell lines were established via lentiviral transduction. Functional assays，including CCK-8，wound healing and Transwell experiments were utilized to evaluate the effects of S100A2 downregulation on CRC cell prolifera- tion，migration，and invasion. Western blot and immunofluorescence staining were employed to analyze the impact of S100A2 knockdown on the expression levels of fructose transporter 5（GLUT5）and ketohexokinase（KHK）. In- tracellular fructose concentration was measured using a fructose assay kit. A nude mouse CRC xenograft model was established using S100A2-knockdown HCT116 cell lines to investigate the role of S100A2 in tumor proliferation in vivo. Tumor tissues from the xenografted mice were analyzed by Western blot and immunofluorescence staining to evaluate the expression levels of GLUT5 and KHK. Results S100A2 expression was significantly elevated in CRC patients compared with healthy individuals. All three CRC cell lines exhibited markedly higher S100A2 expression than normal colonic epithelial cells. S100A2 knockdown significantly inhibited CRC cell proliferation，migration， and invasion capacities. Downregulation of S100A2 suppressed the expression of fructose metabolism-related pro- teins GLUT5 and KHK，accompanied by reduced cellular fructose uptake. In vivo experiments demonstrated that S100A2 knockdown effectively inhibited tumor growth and decreased GLUT5/KHK expression in xenograft tissues. Conclusion Downregulation of S100A2 inhibits CRC progression by modulating fructose metabolism in CRC cells.

The regulatory mechanism of TLR4 on the inflammatory response in mice with gastric ulcers through autophagy and oxidative stress

Du Jinxuan 1，Feiluore Dilixiati 1，Xuan Qiuyun 2

DOI: 10.19405/j.cnki.issn1000-1492.2026.01.006

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abstract:
To investigate the effects of Toll-like receptor 4（TLR4）inhibition on autophagy and oxida‑ tive stress，as well as its regulatory role and mechanism in the inflammatory response in a mouse model of gastric ul ‑ cer. Methods Sixty adult male Kunming mice were equally divided into five groups：control group，model group， model+TLR4-IN-C34 group，model+TLR4-IN-C34+3-MA group，and model+TLR4-IN-C34+H ₂ O ₂ group. Except for the control group，all groups were administered 40 mg/kg indomethacin via gavage. Treatment groups received injections every three days，and all groups were treated for 30 days. Mice were euthanized by cervical dislocation， and gastric tissues were collected. Gastric ulcer scores were assessed，and pathological changes were evaluated via HE staining and scoring. Serum levels of interleukin-1阝（IL-1阝）， IL-6，tumor necrosis factor- α（TNF- α), ad‑ vanced oxidation protein products（AOPP），and prostaglandin E2（PGE2），as well as gastric tissue levels of malo ‑ ndialdehyde（ MDA）， superoxide dismutase（ SOD）， and reduced glutathione（ GSH）， were measured using ELISA. Western blot analysis was performed to detect the expression of TLR4，microtubule-associated protein 1 light chain 3- Ⅰ（LC3- Ⅰ ) , LC3- Ⅱ , autophagy-related protein 5（Atg5），Beclin-1，nuclear factor erythroid 2-re‑ lated factor 2（Nrf2），heme oxygenase-1（HO-1），and NAD（P）H quinone dehydrogenase 1（NQO1）in gastric tis‑ sues. Immunofluorescence staining was used to assess LC3- Ⅱ fluorescence intensity in gastric tissues. Results Compared with the control group，the model group exhibited upregulation of ulcer scores，HE staining scores， TLR4，IL-1阝，IL-6，TNF-α , and AOPP levels，and downregulation of LC3- Ⅱ fluorescence intensity，PGE2 lev‑ els，Atg5，Beclin-1，nuclear Nrf2，HO-1，NQO1 levels，and the LC3- Ⅱ/ Ⅰ ratio（all P < 0. 05）. Compared with the model group，the model+TLR4-IN-C34 group showed downregulation of ulcer scores，HE staining scores， TLR4，IL-1阝，IL-6，TNF-α , and AOPP levels，and upregulation of LC3- Ⅱ fluorescence intensity，PGE2 levels， Atg5，Beclin-1，nuclear Nrf2，HO-1，NQO1 levels，and the LC3- Ⅱ/ Ⅰ ratio（all P < 0. 05）. Compared with the model+TLR4-IN-C34 group，the model+TLR4-IN-C34+3-MA group exhibited upregulation of ulcer scores，HE staining scores，IL-1阝，IL-6，TNF- α , and AOPP levels，and downregulation of LC3- Ⅱ fluorescence intensity， PGE2 levels，Atg5，Beclin-1，and the LC3- Ⅱ/ Ⅰ ratio（all P < 0. 05）. Compared with the model+TLR4-IN-C34 group，the model+TLR4-IN-C34+H₂ O₂ group showed upregulation of ulcer scores，HE staining scores，IL-1阝，IL- 6，TNF-α , and AOPP levels，and downregulation of PGE2 levels and nuclear Nrf2，HO-1，and NQO1 levels（all P < 0. 05）. Conclusion Inhibition of TLR4 ameliorates gastric ulcer symptoms and suppresses the inflammatory response in mice by upregulating autophagy and reducing oxidative stress.

Expression of SLC7A11 in esophageal squamous cell carcinoma tissues and its preliminary study on mediating tumor cell metabolism

Zhang Huakun1，Sun Mengfei2，Sun Qi2，Zhou Ziru1，Yu Jie3，Chen Yunzhao3，Cui Xiaobin1，2

DOI: 10.19405/j.cnki.issn1000-1492.2026.02.012

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abstract:
To investigate the relationship between solute carrier family 7 member 11（SLC7A11）ex- pression in esophageal squamous cell carcinoma（ESCC）and clinical prognosis，and to determine its effects on ESCC cell growth，migration，and other biological activities. Methods SLC7A11 protein expression was mea- sured in 310 ESCC tissues and 259 adjacent normal tissues using immunohistochemistry to statistically assess the association of SLC7A11 with clinicopathologic characteristics and prognosis in ESCC patients. The expression of SLC7A11 in ESCC cell lines was suppressed through siRNA-mediated knockdown. The specific effects of SLC7A11 knockdown on proliferation and migration were evaluated using CCK-8，clonogenic assay，and Transwell assays. Adenosine triphosphate（ATP），lactic acid and pyruvate assays were used to measure ESCC metabolism. Results SLC7A11 protein expression was localized predominantly in the cytoplasm of ESCC tissues. Significantly higher SLC7A11 expression levels were observed in ESCC tissues compared to adjacent normal tissues（P<0. 001）. High SLC7A11 expression was associated with poorer differentiation in patients（P<0. 01）. Kaplan-Meier survival analy- sis demonstrated significantly shorter overall survival in patients with high SLC7A11 expression compared to those with low expression（P<0. 05）. CCK-8 and colony formation assays demonstrated that the knockdown of SLC7A11 expression significantly suppressed the proliferative capacity of tumor cells（P<0. 001）. Furthermore，Transwell assays revealed a marked decline in tumor cell migration capacity following SLC7A11 suppression（P<0. 001）. Critically，SLC7A11 knockdown also reduced intracellular levels of ATP，lactate，and pyruvate，demonstrating that SLC7A11 modulated metabolic activity in ESCC cells（P<0. 001）. Conclusion The expression level of SLC7A11 is relatively high in ESCC and is strongly associated with poor prognosis. Silencing SLC7A11 signifi- cantly inhibits esophageal cancer cell growth and migration. SLC7A11 has the ability to regulate glucose，lactic acid and ATP metabolism levels in ESCC，thereby affecting the metabolic microenvironment of ESCC.

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