Recent advances in deciphering hippocampus complexity using single-cell transcriptomics.

Single-cell and single-nucleus RNA sequencing (scRNA-seq and snRNA-seq) technologies have emerged as revolutionary and powerful tools, which have helped in achieving significant progress in biomedical research over the last decade. scRNA-seq and snRNA-seq resolve heterogeneous cell populations from different tissues and help reveal the function and dynamics at the single-cell level. The hippocampus is an essential component for cognitive functions, including learning, memory, and emotion regulation. However, the molecular mechanisms underlying the activity of hippocampus have not been fully elucidated. The development of scRNA-seq and snRNA-seq technologies provides strong support for attaining an in-depth understanding of hippocampal cell types and gene expression regulation from the single-cell transcriptome profiling perspective. This review summarizes the applications of scRNA-seq and snRNA-seq in the hippocampus to further expand our knowledge of the molecular mechanisms related to hippocampal development, health, and diseases.

RKIP-Mediated NF-κB Signaling is involved in ELF-MF-mediated improvement in AD rat.

In a previous study, we reported the positive effects of extremely low frequency electromagnetic field (ELF-MF) exposure on Alzheimer's disease (AD) rats; however, the underlying mechanism remains unclear. In addition, we found that Raf-1 kinase inhibitor protein (RKIP) was downregulated by microwave exposure in the rat hippocampus. Our hypothesis was that RKIP-mediated NF-κB pathway signaling is involved in the effect of ELF-MF on the AD rat. In this study, D-galactose intraperitoneal (50 mg/kg/d for 42 d) and Aß25-35 hippocampal (5 µL/unilateral, bilateral, single-dose) injection were implemented to establish an AD rat model. Animals were exposed to 50 Hz and 400 µT ELF-MF for 60 continuous days. The spatial memory ability of the rat was then tested using the Morris water maze. Protein expression and interaction were detected by western blotting and co-immunoprecipitation for RKIP-mediated NF-κB pathway factors. The results showed that ELF-MF exposure partially improved the cognitive disorder, upregulated the levels of RKIP, TAK1, and the RKIP/TAK1 interaction, but downregulated p-IKK levels in AD rats. These results indicated that RKIP-mediated NF-κB pathway signaling plays an important role in the ELF-MF exposure-mediated improvements in the AD rat. Our study suggested that ELF-MF exposure might have a potential therapeutic value for AD. Further in depth studies are required in the future.

Neural cell apoptosis induced by microwave exposure through mitochondria-dependent caspase-3 pathway.

To determine whether microwave (MW) radiation induces neural cell apoptosis, differentiated PC12 cells and Wistar rats were exposed to 2.856 GHz for 5 min and 15 min, respectively, at an average power density of 30 mW/cm². JC-1 and TUNEL staining detected significant apoptotic events, such as the loss of mitochondria membrane potential and DNA fragmentation, respectively. Transmission electron microscopy and Hoechst staining were used to observe chromatin ultrastructure and apoptotic body formation. Annexin V-FITC/PI double staining was used to quantify the level of apoptosis. The expressions of Bax, Bcl-2, cytochrome c, cleaved caspase-3 and PARP were examined by immunoblotting or immunocytochemistry. Caspase-3 activity was measured using an enzyme-linked immunosorbent assay. The results showed chromatin condensation and apoptotic body formation in neural cells 6h after microwave exposure. Moreover, the mitochondria membrane potential decreased, DNA fragmentation increased, leading to an increase in the apoptotic cell percentage. Furthermore, the ratio of Bax/Bcl-2, expression of cytochrome c, cleaved caspase-3 and PARP all increased. In conclusion, microwave radiation induced neural cell apoptosis via the classical mitochondria-dependent caspase-3 pathway. This study may provide the experimental basis for further investigation of the mechanism of the neurological effects induced by microwave radiation.

[Microwave radiation induces injury to GC-2spd cells].

OBJECTIVE: To explore the impact of microwave radiation on GC-2spd cells. METHODS: We exposed cultured GC-2spd cells to microwave radiation at the average power densities of 0, 10 and 30 mW/cm2 for 15 minutes and, from I to 24 hours after the exposure, we observed the changes in cell proliferation, histology and ultrastructure, cell apoptosis, and cAMP content by MTIT, light microscopy, electron microscopy, flow cytometry and ELISA. RESULTS: Compared with the control group, the GC-2spd cells showed a significant decrease in proliferation ability at 1 -24 hours after 10 and 30 mW/cm2 microwave radiation, except at 12 hours after 30 mW/cm2 radiation (P <0.05 or P <0.01), with reduced length and number of cell enation and increased intra cytoplasm vacuoles. The rate of cell apoptosis (%) was significantly increased in the 10 and 30 mW/cm2 groups at 6 hours (4.56 +/- 2.09 vs 14.59 +/- 1.09 and 8.48 +/- 1.73, P <0.05 or P <0.01) , with agglutination and margin translocation of chromatins and obvious dilation of endo cytoplasmic reticula. The cAMP content (nmol/g) in the GC-2spd cells was remarkably reduced in the 10 and 30 mW/cm2 groups at 6 and 24 hours (2.77 +/-0.24 vs 1.65+/- 0. 17 and 1.96+/-0.10, 3.02 +/-0.47 vs 2.13 +/-0.33 and 1.69 +/-0.27, P <0.05 or P <0.01). CONCLUSION: Microwave radiation at 10 and 30 mW/cm2 may cause injury to GC-2spd cells, which is manifested by decreased content of intracellular cAMP, reduced activity of cell proliferation, and increased rate of cell apoptosis.

Rhabdomyolysis-induced acute kidney injury under hypoxia and deprivation of food and water.

BACKGROUND: To investigate the renal pathophysiologyin rhabdomyolysis-induced acute kidney injury (AKI) in rats under hypoxia and deprivation of food and water (HDFW), thus broadening the knowledge about rhabdomyolysis-induced AKI in massive earthquake. METHODS: Male Wistar rats weighing 200-230g were randomized into control, rhabdomyolysis (R), HDFW and rhabdomyolysis in combination with HDFW (R/HDFW) group. Experimental rhabdomyolysis rat model was established through clamping hind limb muscles, HDFW model rats were kept in 10% hypoxic chamber unavailable to food and water. At 1, 3, 5, 7, 9, 11d after treatment, serum creatinine (Scr) level, renal index, renal structural changes and cell apoptosis were analyzed. RESULTS: After R, HDFW, R/HDFW treatment, the animals showed significantly higher Scr levels than the control group. Renal index in R and R/HDFW groups elevated remarkably compared with that in control and HDFW group. The results of histopathology, ultra-structure and apoptosis assay suggested that rhabdomyolysis caused renal tubular injury, HDFW treatment resulted in renal vascular dilation, tissue congestion and tubular cell damage. In addition, more severe renal lesion appeared in R/HDFW. CONCLUSIONS: We conclude that the association of experimental rhabdomyolysis with HDFW results in a different functional and histological pattern. The rhabdomyolysis-HDFW combination causes more severe renal injury.

Microarray analysis of altered gene expression and the role of ATF3 in HK-2 cells treated with hemin.

OBJECTIVE: To identify gene expression changes and the role of activating transcription factor 3 (ATF3) in hemin toxicity in renal tubular epithelial cells, then elucidate molecular mechanisms of hemin toxicity on renal tubular epithelial cells. METHODS: An oligo array comprising 35,035 genes was used to compare differential gene expression in hemin-treated and non-treated HK-2 cells (human renal proximal tubular epithelial cells), and the role of ATF3 in hemin toxicity was assessed using siRNA technique. RESULTS: A total of 128 mRNAs were at least twofold up-regulated and 101 mRNAs were at least twofold down-regulated after hemin treatment. Expression levels of ATF3, heat shock protein 70, c-fos, and c-jun were remarkably increased. Hemin also suppressed nuclear factor-kappa B inhibitor α, ß-2 adrenergic receptor, and interleukin-6 mRNA amounts more than twofold. We further demonstrated the protective role of ATF3 in hemin cytotoxicity. CONCLUSIONS: The data suggest that hemin caused multiple changes of gene expression in HK-2 cells, and ATF3 protects against hemin cytotoxicity.

[Changes in Ca(2+)concentration and caspase-3 expression and their relationship in Raji cells exposed to electromagnetic radiation].

OBJECTIVE: To study the effects of electromagnetic pulse (EMP), S-band high power microwave (S-HPM), and X-band high power microwave (X-HPM) on the Ca(2+) concentration and caspase-3 expression in Raji cells and the relationship between Ca(2+) concentration and caspase-3 expression, and to investigate the regulatory mechanism of electromagnetic radiation damage. METHODS: Raji cells were cultured conventionally. Some cells were irradiated by EMP, S-HPM, and X-HPM in the logarithmic growth phase for 6 hours and then collected; others received sham irradiation as a control. The Ca(2+) concentration in the cells was measured by laser scanning confocal microscope; the caspase-3 expression in the cells was evaluated by Western blot. RESULTS: Compared with the control group (Ca(2+) fluorescence intensity = 43.08 ± 2.08; caspase-3 expression level = 0.444 ± 0.13), the EMP,S-HPM, and X-HPM groups had significantly increased Ca(2+) concentrations, with Ca(2+) fluorescence intensities of 69.56 ± 1.71, 50.06 ± 1.89, and 70.68 ± 1.59, respectively (P < 0.01), and had upregulated caspase-3 expression, with expression levels of 0.964 ± 0.12, 0.586 ± 0.16, and 0.970 ± 0.07, respectively (P < 0.01). Each of the EMP and X-HPM groups had significantly higher Ca(2+) fluorescence intensity and caspase-3 expression level than the S-HPM group (P < 0.01), but there were no significant differences between the EMP and X-HPM groups. The linear regression analysis showed that the caspase-3 expression was upregulated as the Ca(2+) concentration increased, with a positive correlation between them (P < 0.01). CONCLUSION: EMP, S-HPM, and X-HPM cause damage probably by increasing the Ca(2+) concentration in cells and in turn inducing caspase-3 overexpression.

Advances in the study of cholinergic circuits in the central nervous system.

OBJECTIVE: Further understanding of the function and regulatory mechanism of cholinergic neural circuits and related neurodegenerative diseases. METHODS: This review summarized the research progress of the central cholinergic nervous system, especially for the cholinergic circuit of the medial septal nucleus-hippocampus, vertical branch of diagonal band-hippocampus, basal nucleus of Meynert-cerebral cortex cholinergic loop, amygdala, pedunculopontine nucleus, and striatum-related cholinergic loops. RESULTS: The extensive and complex fiber projection of cholinergic neurons form the cholinergic neural circuits, which regulate several nuclei in the brain through neurotransmission and participate in learning and memory, attention, emotion, movement, etc. The loss of cholinergic neurotransmitters, the reduction, loss, and degeneration of cholinergic neurons or abnormal theta oscillations and cholinergic neural circuits can induce cognitive disorders such as AD, PD, PDD, and DLB. INTERPRETATION: The projection and function of cholinergic fibers in some nuclei and the precise regulatory mechanisms of cholinergic neural circuits in the brain remain unclear. Further investigation of cholinergic fiber projections in various brain regions and the underlying mechanisms of the neural circuits are expected to open up new avenues for the prevention and treatment of senile neurodegenerative diseases.

Effects of Nonthermal Radiofrequency Stimulation on Neuronal Activity and Neural Circuit in Mice.

Whether the nonthermal effects of radiofrequency radiation (RFR) exist and how nonthermal RFR acts on the nervous system are unknown. An animal model of spatial memory impairment is established by exposing mice to 2856-MHz RFR in the range of thermal noise (≤1 °C). Glutamate release in the dorsal hippocampus (dHPC) CA1 region is not significantly changed after radiofrequency exposure, whereas dopamine release is reduced. Importantly, RFR enhances glutamatergic CA1 pyramidal neuron calcium activity by nonthermal mechanisms, which recover to the basal level with RFR termination. Furthermore, suppressed dHPC dopamine release induced by radiofrequency exposure is due to decreased density of dopaminergic projections from the locus coeruleus to dHPC, and artificial activation of dopamine axon terminals or D1 receptors in dHPC CA1 improve memory damage in mice exposed to RFR. These findings indicate that nonthermal radiofrequency stimulation modulates ongoing neuronal activity and affects nervous system function at the neural circuit level.

Single-cell map of dynamic cellular microenvironment of radiation-induced intestinal injury.

Intestine is a highly radiation-sensitive organ that could be injured during the radiotherapy for pelvic, abdominal, and retroperitoneal tumors. However, the dynamic change of the intestinal microenvironment related to radiation-induced intestine injury (RIII) is still unclear. Using single-cell RNA sequencing, we pictured a dynamic landscape of the intestinal microenvironment during RIII and regeneration. We showed that the various cell types of intestine exhibited heterogeneous radiosensitivities. We revealed the distinct dynamic patterns of three subtypes of intestinal stem cells (ISCs), and the cellular trajectory analysis suggested a complex interconversion pattern among them. For the immune cells, we found that Ly6c+ monocytes can give rise to both pro-inflammatory macrophages and resident macrophages after RIII. Through cellular communication analysis, we identified a positive feedback loop between the macrophages and endothelial cells, which could amplify the inflammatory response induced by radiation. Besides, we identified different T cell subtypes and revealed their role in immunomodulation during the early stage of RIII through inflammation and defense response relevant signaling pathways. Overall, our study provides a valuable single-cell map of the multicellular dynamics during RIII and regeneration, which may facilitate the understanding of the mechanism of RIII.

Application of 1H-NMR-based metabolomics for detecting injury induced by long-term microwave exposure in Wistar rats' urine.

There has been growing public concern regarding exposure to microwave fields as a potential human health hazard. This study aimed to identify sensitive biochemical indexes for the detection of injury induced by microwave exposure. Male Wistar rats were exposed to microwaves for 6 min per day, 5 days per week over a period of 1 month at an average power density of 5 mW/cm(2) (specific absorption rate of 2.1 W/kg). Urine specimens were collected over 24 h in metabolic cages at 7 days, 21 days, 2 months, and 6 months after exposure. (1)H NMR spectroscopy data were analyzed using multivariate statistical techniques. Urine metabolic profiles of rats after long-term microwave exposure were significantly differentiated from those of sham-treated controls using principal component analysis or partial least squares discriminant analysis. Significant differences in low molecular weight metabolites (acetate, succinate, citrate, ketoglutarate, glucose, taurine, phenylalanine, tyrosine, and hippurate) were identified in the 5 mW/cm(2) microwave exposure group compared with the sham-treated controls at 7 days, 21 days, and 2 months. Metabolites returned to normal levels by 6 months after exposure. These data indicated that these metabolites were related to the perturbations of energy metabolism particularly in the tricarboxylic acid cycle, and the metabolism of amino acids, monoamines, and choline in urine represent potential indexes for the detection of injury induced by long-term microwave exposure.

Effects of the continuous pulsation regeneration on the soot combustion in diesel particulate filter for heavy-duty truck.

Continuous pulsation regeneration combustion of soot is employed for sine and cosine simulation study. Data showed that pressure uniformity of sine condition is better than that of cosine condition with the maximum pressure difference of 4353.5 Pa under the same simulation boundary conditions. The maximum regeneration temperature under cosine pressure is 46.12 K which is higher than that in sine form. Regeneration combustion reaction zone tends to be more stable laminar flow and Reynolds number of sine condition is 435.23 less than that of under cosine condition. The maximum Stanton number of cosine pressure condition is 3.67 and that of sine pressure condition is 5.15, which investigates heat transfer capacity of the sine pressure condition is better than that of the pressure of cosine form. The regeneration efficiency of inlet gradually increased from the minimum regeneration efficiency 74.18%-88.45% of sine and cosine. The soot under both pressure forms has achieved complete regeneration and the regeneration efficiency has exceeded 88% of porous medium filter body section. The soot regeneration combustion efficiency of the porous media filter section and outlet section is more sufficient under sine condition and the heat carried by the fluid can maintain the soot regeneration.

Single-Cell RNA Sequencing for Analyzing the Intestinal Tract in Healthy and Diseased Individuals.

The intestinal tract is composed of different cell lineages with distinct functions and gene expression profiles, providing uptake of nutrients and protection against insults to the gut lumen. Changes in or damage to the cellulosity or local environment of the intestinal tract can cause various diseases. Single-cell RNA sequencing (scRNA-seq) is a powerful tool for profiling and analyzing individual cell data, making it possible to resolve rare and intermediate cell states that are hardly observed at the bulk level. In this review, we discuss the application of intestinal tract scRNA-seq in identifying novel cell subtypes and states, targets, and explaining the molecular mechanisms involved in intestinal diseases. Finally, we provide future perspectives on using single-cell techniques to discover molecular and cellular targets and biomarkers as a new approach for developing novel therapeutics for intestinal diseases.

Chronic stress model simulated by salbutamol promotes tumorigenesis of gastric cancer cells through ß2-AR/ERK/EMT pathway.

Chronic stress induced by long-term anxiety and depression can promote the malignant progression of gastric cancer. ß2-adrenergic receptor (ß2-AR) is a critical mediator for chronic stress-induced multiple processes of tumor cells. However, the function of chronic stress in gastric cancer and its potential mechanisms in vivo and in vitro, especially at the cellular level, remain unknown. Here, we provide further evidence that chronic stress affected behavior and hypothalamus pituitary adrenal axis related hormone levels in mice. Furthermore, immunofluorescence showed that emotion affected the expression of epithelial-mesenchymal transition (EMT) markers in patients' tissues. To address this, salbutamol, a specific agonist of ß2-AR, was utilized for simulating chronic stress and demonstrating the mechanism of stress in tumor progression at the molecular level both in vivo and in vitro. Salbutamol significantly induced EMT, migration and invasion via ERK (Extracellular-signal-regulated kinase) phosphorylation, and the effects were reversed by the ß2-AR antagonist ICI-118,551. The promoting effects of salbutamol on EMT, migration and invasion were inhibited by phosphorylation inhibitor of ERK PD98059 in vitro. Analysis of xenograft models revealed that salbutamol significantly promoted tumor growth and adrenal volume, while ICI-118,551 inhibited these effects. In addition, salbutamol increased the expression of mesenchymal marker N-cadherin and decreased epithelial marker E-cadherin in transplanted tumor tissue. In conclusion, salbutamol simulates a chronic stress model, which promotes tumorigenesis of gastric cancer cells through ß2-AR/ERK/EMT pathway.

High-Power Electromagnetic Pulse Exposure of Healthy Mice: Assessment of Effects on Mice Cognitions, Neuronal Activities, and Hippocampal Structures.

Electromagnetic pulse (EMP) is a high-energy pulse with an extremely rapid rise time and a broad bandwidth. The brain is a target organ sensitive to electromagnetic radiation (EMR), the biological effects and related mechanisms of EMPs on the brain remain unclear. The objectives of the study were to assess the effects of EMP exposure on mouse cognitions, and the neuronal calcium activities in vivo under different cases of real-time exposure and post exposure. EMP-treated animal model was established by exposing male adult C57BL/6N mice to 300 kV/m EMPs. First, the effects of EMPs on the cognitions, including the spatial learning and memory, avoidance learning and memory, novelty-seeking behavior, and anxiety, were assessed by multiple behavioral experiments. Then, the changes in the neuronal activities of the hippocampal CA1 area in vivo were detected by fiber photometry in both cases of during real-time EMP radiation and post-exposure. Finally, the structures of neurons in hippocampi were observed by optical microscope and transmission electron microscope. We found that EMPs under this condition caused a decline in the spatial learning and memory ability in mice, but no effects on the avoidance learning and memory, novelty-seeking behavior, and anxiety. The neuron activities of hippocampal CA1 were disturbed by EMP exposure, which were inhibited during EMP exposure, but activated immediately after exposure end. Additionally, the CA1 neuron activities, when mice entered the central area in an Open field (OF) test or explored the novelty in a Novel object exploration (NOE) test, were inhibited on day 1 and day 7 after radiation. Besides, damaged structures in hippocampal neurons were observed after EMP radiation. In conclusion, EMP radiation impaired the spatial learning and memory ability and disturbed the neuronal activities in hippocampal CA1 in mice.

[Long-term microwave radiation affects male reproduction in rats].

OBJECTIVE: To investigate the effect of long-term microwave radiation on male reproduction in rats. METHODS: A total of 100 male Wistar rats were exposed to microwave radiation with average power density of 0, 2.5, 5 and 10 mW/cm2 for 4 weeks, 5 times a week and 6 minutes per time. Changes in serum testosterone, testicular index, histology and ultrastructure, and the percentage of teratospermia in the epididymis were observed dynamically at 6 h, 7 d, 14 d, 28 d and 60 d after the exposure. RESULTS: There was a significant decrease in serum testosterone concentration at 28 d after microwave radiation at 2.5, 5 and 10 mW/cm2 ([10.20 +/- 4.31] ng/ml, [5.56 +/- 3.47] ng/ml and [7.53 +/- 4.54] ng/ml) and at 60 d at 10 mW/cm2 ( [15.95 +/- 9.54] ng/ml), as compared with the control group ([23.35 +/- 8.06] ng/ml and [31.40 +/- 9.56] ng/ml) (P < 0.05 or P < 0.01). No significant changes were found in the testis index at 6 h -60 d after microwave radiation at the three doses, but different degrees of degeneration, necrosis and shedding of spermatogenic cells, thinning of spermatogenic epithelia, and decrease or deletion of spermatozoa were observed, and more obvious at 28 d and 60 d. Swelling and cavitation of mitochondria in all spermatogenic cells, agglutination and margin translocation of nuclear chromatin in the spermatogonial and Leydig cells were seen at 7 d and 60 d after 5 mW/cm2 microwave radiation. The rate of teratospermia of the epididymis was increased, more obviously at 7 d after 2.5, 5 mW/cm2, 60 d after 5 mW/cm2, and 7 d, 28 d and 60 d after 10 mW/cm2 microwave radiation (P < 0.05 or P < 0.01). CONCLUSION: Long-term microwave radiation may cause injury to male reproduction, which is positively correlated with the radiation dose, and has an obvious late effect.

Progress on the Function and Application of Thymosin ß4.

Thymosin ß4 (Tß4) is a multifunctional and widely distributed peptide that plays a pivotal role in several physiological and pathological processes in the body, namely, increasing angiogenesis and proliferation and inhibiting apoptosis and inflammation. Moreover, Tß4 is effectively utilized for several indications in animal experiments or clinical trials, such as myocardial infarction and myocardial ischemia-reperfusion injury, xerophthalmia, liver and renal fibrosis, ulcerative colitis and colon cancer, and skin trauma. Recent studies have reported the potential application of Tß4 and its underlying mechanisms. The present study reveals the progress regarding functions and applications of Tß4.

Effects of Radiofrequency Electromagnetic Radiation on Neurotransmitters in the Brain.

With the rapid development of electronic information in the past 30 years, technical achievements based on electromagnetism have been widely used in various fields pertaining to human production and life. Consequently, electromagnetic radiation (EMR) has become a substantial new pollution source in modern civilization. The biological effects of EMR have attracted considerable attention worldwide. The possible interaction of EMR with human organs, especially the brain, is currently where the most attention is focused. Many studies have shown that the nervous system is an important target organ system sensitive to EMR. In recent years, an increasing number of studies have focused on the neurobiological effects of EMR, including the metabolism and transport of neurotransmitters. As messengers of synaptic transmission, neurotransmitters play critical roles in cognitive and emotional behavior. Here, the effects of EMR on the metabolism and receptors of neurotransmitters in the brain are summarized.

mmu-miR-145a-5p Accelerates Diabetic Wound Healing by Promoting Macrophage Polarization Toward the M2 Phenotype.

Diabetic wounds are recalcitrant to healing. One of the important characteristics of diabetic trauma is impaired macrophage polarization with an excessive inflammatory response. Many studies have described the important regulatory roles of microRNAs (miRNAs) in macrophage differentiation and polarization. However, the differentially expressed miRNAs involved in wound healing and their effects on diabetic wounds remain to be further explored. In this study, we first identified differentially expressed miRNAs in the inflammation, tissue formation and reconstruction phases in wound healing using Illumina sequencing and RT-qPCR techniques. Thereafter, the expression of musculus (mmu)-miR-145a-5p ("miR-145a-5p" for short) in excisional wounds of diabetic mice was identified. Finally, expression of miR-145a-5p was measured to determine its effects on macrophage polarization in murine RAW 264.7 macrophage cells and wound healing in diabetic mice. We identified differentially expressed miRNAs at different stages of wound healing, ten of which were further confirmed by RT-qPCR. Expression of miR-145a-5p in diabetic wounds was downregulated during the tissue formation stage. Furthermore, we observed that miR-145a-5p blocked M1 macrophage polarization while promoting M2 phenotype activation in vitro. Administration of miR-145a-5p mimics during initiation of the repair phase significantly accelerated wound healing in db/db diabetic mice. In conclusion, our findings suggest that rectifying macrophage function using miR-145a-5p overexpression accelerates diabetic chronic wound healing.

[Microwave radiation decreases the expressions of occludin and JAM-1 in rats].

OBJECTIVE: To explore the changes in the expressions of the tight junction related protein occludin and junctional adhesion molecule-1 (JAM-1) of the blood-testis barrier and their significance in rats after microwave radiation. METHODS: Eighty male Wistar rats were exposed to microwave radiation with average power density of 0, 10, 30 and 100 mW/cm2 for five minutes, and dynamic changes in the expressions of testicular occludin and JAM-1 were observed by Western blot and image analysis at 6 h, 1 d, 3 d, 7 d and 14 d after the radiation. RESULTS: There was a significant down-regulation in the expression of the occludin protein at 3 - 7 d, 6 h - 7 d and 6 h - 14 d (P < 0. 05), as well as in that of JAM-1 at 3 - 7 d, 1 - 7 d and 1-14 d (P < 0.05) after exposure to 10, 30 and 100 mW/cm2 microwave radiation. CONCLUSION: The decreased protein expressions of occludin and JAM-1 may play an important role in the microwave radiation induced-damage to the blood-testis barrier.