Diabetic nephropathy is the most serious complication of diabetes and a major cause of end-stage renal disease worldwide.Although hyperglycaemia is widely considered to be the main driving force for the progression of diabetic nephropathy to end-stage renal disease,inflammatory signaling pathways and inflammatory cells also play important roles in the pathogenesis and progression of the disease.Therefore,treatment strategies targeting the inflammation-related intracellular signaling pathways may become a new direction for the treatment of diabetic nephropathy.Currently,the development of anti-inflammatory drugs for diabetic nephropathy is also underway,and they have shown promising results in experimental models.This article focuses on the connection between inflammatory cells and inflammatory signaling pathways and diabetic nephropathy,as well as the current research progress on targeted anti-inflammatory treatment.

Objective:To explore the expression of NLRP3 inflammatory vesicles in hippocampal tissue and prefron-tal cortex in a mouse model of posttraumatic stress disorder(PTSD).Methods:Male C57BL/6J mice were randomly divided into 2 groups:the control group and the PTSD group.The PTSD group used conditioned foot shock(CF)and single-sustained stress(SPS)to prepare an animal model of PTSD.Anxiety and depression responses of the mouse mod-el were detected by the open field experiment and elevated cross maze test.Memory and memory capacity tests were es-tablished by the darkness-avoidance experimental system.Morphological changes in the hippocampus and prefrontal cor-tex of mice were observed by hematoxylin-eosin staining(HE),and the expression of NLRP3 inflammatory vesicles was detected using Western Blot and immunohistochemical staining.Results:The PTSD mouse group showed decreased body mass,anxiety and depression-like behaviors,and decreased learning and memory abilities compared with the con-trol group(P＜0.05).HE staining showed tissue damage in the hippocampal CA1 region and prefrontal cortex in PTSD mice compared with the control group.Western Blot and immunohistochemical staining showed that after 3 d of PTSD stimulation,hippocampal and prefrontal cortical NLRP3 inflammatory vesicles were activated(P＜0.05).Conclusion:Increased expression of NLRP3 inflammatory vesicles in the hippocampus and prefrontal cortex of PTSD model mice.

Objective:To investigate the application value of nectin-4 targeting radiotracer 68Ga-N188 in the diagnosis of pancreatic cancer. Methods:The prospective study was conducted. The clinicopathologic data of 16 patients diagnosed as pancreatic cancer on enhanced computed tomography (CT) who were admitted to the Peking University First Hospital from August to December 2022 were collected. There were 9 males and 7 females, aged (62±8)years. All patients underwent 18F-flurodeoxyglucose ( 18F-FDG) and 68Ga-N188 positron emission tomography (PET)/CT examination. Observation indicators: (1) distribution of 68Ga-N188 in different tissues and tumor primary lesion of patients; (2) expression of Nectin-4 and uptake of 68Ga-N188 in pancreatic cancer; (3) comparison of examination results between 68Ga-N188 and 18F-FDG PET/CT. Measurement data with normal distribution were represented as Mean± SD, and comparison between groups was conducted using the independent sample t test. Count data were described as absolute numbers or percentages. Results:(1) Distribution of 68Ga-N188 in different tissues and tumor primary lesion of patients. Results of PET/CT examination showed that in 1 hour after injection, the maximum standard uptake value (SUVmax) and mean standard uptake value (SUVmean) of 68Ga-N188 in fat, muscle, skin, and brain tissues of 16 patients were 0.40±0.16 and 0.25±0.09, 0.68±0.20 and 0.44±0.12, 0.39±0.14 and 0.28±0.11, 0.09±0.04 and 0.05±0.02, respectively. In the tissues of the esophagus, liver, spleen, and pancreas, the above indicators were 1.53±0.48 and 1.16±0.31, 1.49±0.45 and 0.91±0.30, 1.40±0.30 and 1.02±0.24, 1.24±0.31 and 0.96±0.25, respectively. In tumor primary lesion, the above indicators were 3.28±1.02 and 2.14±0.62, respectively, showing significant differences in SUVmax and SUVmean compared with pancreatic tissue ( t=8.03, 6.75, P<0.05). The tumor background ratio in tumor primary lesion based on SUVmax was 1.82±0.58. (2) Expression of Nectin-4 and uptake of 68Ga-N188 in pancreatic cancer. Results of immunohistochemical staining in 16 patients showed that there were 7 patients with high Nectin-4 expression and 9 patients with low Nectin-4 expression. Results of PET/CT examination showed that the SUVmax of 68Ga-N188 in tumor primary lesion of the 7 patients with high Nectin-4 expression and 9 patients with low Nectin-4 expression were 3.77±1.10 and 2.64±0.68, showing a significant difference between them ( t=2.64, P<0.05). The SUVmax of 18F-FDG in tumor primary lesion of the 7 patients with high Nectin-4 expression and 9 patients with low Nectin-4 expression were 6.73±3.24 and 6.43±3.45, showing no significant difference between them ( t=0.17, P>0.05). (3) Comparison of examination results between 68Ga-N188 and 18F-FDG PET/CT. Of the 16 patients, cases with positive results of tumor primary lesion on 68Ga-N188 and 18F-FDG PET/CT were 14 and 11, respectively, for the 14 pancreatic cancer patients diagnosed by postoperative histopathology. Among them, cases with positive results of tumor primary lesion on 68Ga-N188 and 18F-FDG PET/CT were 3 and 1 for the 3 pancreatic cancer patients receiving evaluation for chemotherapy. The SUVmax of 18F-FDG in tumor primary lesion of the 3 patients with chemotherapy and the 11 patients without chemotherapy were 2.80±0.69 and 6.97±2.11, showing a significant difference between them ( t=3.29, P<0.05). The SUVmax of 68Ga-N188 in tumor primary lesion of the 3 patients with chemotherapy and the 11 patients without chemotherapy were 3.38±1.12 and 2.93±0.50, showing no significant difference between them ( t=0.66, P>0.05). Cases with positive results of lymph node metastases in 68Ga-N188 and 18F-FDG PET/CT were 6 and 4, respectively, for the 6 pancreatic cancer patients diagnosed with lymph node metastases by postoperative histopathology, and the SUVmax of 68Ga-N188 and 18F-FDG in lymph node metastases were 2.25±1.12 and 4.02±1.27. Conclusion:68Ga-N188 PET/CT can be used for imaging diagnosis of tumor primary lesion and lymph node metastases of pancreatic cancer.

Myocardial injury (MI) is a common occurrence in clinical practice caused by various factors such as ischemia, hypoxia, infection, metabolic abnormalities, and inflammation. Such damages are characterized by a reduction in myocardial function and cardiomyocyte death that can result in dangerous outcomes such as cardiac failure and arrhythmias. An endoplasmic reticulum stress (ERS)-induced unfolded protein response (UPR) is triggered by several stressors, and its intricate signaling networks are instrumental in both cell survival and death. Cardiac damage frequently triggers ERS in response to different types of injuries and stress. High levels of ERS can exacerbate myocardial damage by inducing necrosis and apoptosis. To target ERS in MI prevention and treatment, current medical research is focused on identifying effective therapy approaches. Traditional Chinese medicine (TCM) is frequently used because of its vast range of applications and low risk of adverse effects. Various studies have demonstrated that active components of Chinese medicines, including polyphenols, saponins, and alkaloids, can reduce myocardial cell death, inflammation, and modify the ERS pathway, thus preventing and mitigating cardiac injury. Thus, this paper aims to provide a new direction and scientific basis for targeting ERS in MI prevention and treatment. We specifically summarize recent research progress on the regulation mechanism of ERS in MI by active ingredients of TCM.

Myocardial injury(MI)is a common occurrence in clinical practice caused by various factors such as ischemia,hypoxia,infection,metabolic abnormalities,and inflammation.Such damages are character-ized by a reduction in myocardial function and cardiomyocyte death that can result in dangerous out-comes such as cardiac failure and arrhythmias.An endoplasmic reticulum stress(ERS)-induced unfolded protein response(UPR)is triggered by several stressors,and its intricate signaling networks are instrumental in both cell survival and death.Cardiac damage frequently triggers ERS in response to different types of injuries and stress.High levels of ERS can exacerbate myocardial damage by inducing necrosis and apoptosis.To target ERS in MI prevention and treatment,current medical research is focused on identifying effective therapy approaches.Traditional Chinese medicine(TCM)is frequently used because of its vast range of applications and low risk of adverse effects.Various studies have demonstrated that active components of Chinese medicines,including polyphenols,saponins,and al-kaloids,can reduce myocardial cell death,inflammation,and modify the ERS pathway,thus preventing and mitigating cardiac injury.Thus,this paper aims to provide a new direction and scientific basis for targeting ERS in MI prevention and treatment.We specifically summarize recent research progress on the regulation mechanism of ERS in MI by active ingredients of TCM.

Objective:To explore the expression of NLRP3 inflammatory vesicles in hippocampal tissue and prefron-tal cortex in a mouse model of posttraumatic stress disorder(PTSD).Methods:Male C57BL/6J mice were randomly divided into 2 groups:the control group and the PTSD group.The PTSD group used conditioned foot shock(CF)and single-sustained stress(SPS)to prepare an animal model of PTSD.Anxiety and depression responses of the mouse mod-el were detected by the open field experiment and elevated cross maze test.Memory and memory capacity tests were es-tablished by the darkness-avoidance experimental system.Morphological changes in the hippocampus and prefrontal cor-tex of mice were observed by hematoxylin-eosin staining(HE),and the expression of NLRP3 inflammatory vesicles was detected using Western Blot and immunohistochemical staining.Results:The PTSD mouse group showed decreased body mass,anxiety and depression-like behaviors,and decreased learning and memory abilities compared with the con-trol group(P＜0.05).HE staining showed tissue damage in the hippocampal CA1 region and prefrontal cortex in PTSD mice compared with the control group.Western Blot and immunohistochemical staining showed that after 3 d of PTSD stimulation,hippocampal and prefrontal cortical NLRP3 inflammatory vesicles were activated(P＜0.05).Conclusion:Increased expression of NLRP3 inflammatory vesicles in the hippocampus and prefrontal cortex of PTSD model mice.