Anti-Human CD68 FITC 25 tests
- Known as:
- Antibody toHuman CD68 fluorecein 25 tests
- Catalog number:
- 11-0689-71
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD68 FITC 25 tests
Related genes to: Anti-Human CD68 FITC 25 tests
- Gene:
- CD68 NIH gene
- Name:
- CD68 molecule
- Previous symbol:
- -
- Synonyms:
- SCARD1, macrosialin, GP110, DKFZp686M18236, LAMP4
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-11
- Date modifiied:
- 2016-10-05
Related products to: Anti-Human CD68 FITC 25 tests
Related articles to: Anti-Human CD68 FITC 25 tests
- Nephrotic syndrome, characterised by proteinuria and hypoalbuminaemia, is caused by the dysregulation of glomerular podocytes and is a significant contributor to chronic kidney disease (CKD). Sympathetic neurotransmitter noradrenaline, acting through adrenoceptor signalling, contributes to progression of various diseases, including CKD. We previously reported that treatment with yohimbine, an α2-adrenoceptor antagonist, decreased urinary protein excretion in 5/6 nephrectomy-induced CKD rat model and that α2-adrenoceptors are localised in podocytes. This suggested that noradrenaline may induce proteinuria via α2-adrenoceptors in podocytes. Therefore, this study investigated the renoprotective effects of yohimbine in puromycin aminonucleoside (PAN)-induced nephrotic syndrome. Male Sprague-Dawley rats were randomly allocated to sham-operated, PAN (50 mg/kg, i.v.), and PAN + yohimbine (3 mg/L in drinking water) groups. PAN group exhibited increased urinary protein, decreased plasma protein, and increased urinary and plasma noradrenaline levels compared to sham group. Furthermore, pronounced infiltration of CD68-positive cells was observed in the PAN group. The expression levels of the podocyte markers podocin and nephrin were lower in PAN rats than in control rats. Conversely, podocytes in PAN rats exhibited increased desmin, transforming growth factor (TGF)-β1, and cleaved caspase 3 expressions along with higher prevalence of apoptotic cells. Treatment with yohimbine reduced proteinuria and hypoalbuminemia, along with suppressing the downregulation of podocin expression. Furthermore, yohimbine suppressed the expression of desmin, TGF-β1, cleaved caspase-3, and apoptotic cells in glomeruli. Administration of yohimbine reduced the infiltration of CD68-positive cells in the kidney tissue. Collectively, these findings suggest that noradrenaline may promote podocyte injury in PAN-induced nephrotic syndrome via α2-adrenoceptors. - Source: PubMed
Publication date: 2026/09/18
Shimokawa TakaomiIwamoto AkariTamura Yasuhisa - This review examines metabolic comorbidities affecting the heart, liver and kidney. The clinical prevalence of cardiohepatorenal metabolic comorbidities associated with obesity and type 2 diabetes is substantial. Chronic low-grade inflammation serves as the fundamental pathogenic mechanism. Abnormal macrophage activation is associated with metabolic disorders and damage to multiple organs. The conventional M1/M2 binary classification fails to adequately capture the heterogeneity of macrophages in vivo. Previous studies have primarily focused on the investigation of individual organs, leaving the cross-organ immune-metabolic linkage mechanism poorly understood. Furthermore, targeted interventions often lack precision. In this study, we systematically summarize the roles of macrophage polarization, phenotypic remodeling and metabolic activation in the injury of three metabolic organs. We also analyze their mediating functions in inter-organ immune-metabolic crosstalk and the associated pathological connections. Glycolipid toxicity impairs the glycolipid metabolism of macrophages via the NLRP3/SIRT pathway, resulting in a pro-inflammatory polarization advantage. Specific subsets of macrophages, including CCR2,TREM2,and CD206CD68,are involved in mediating myocardial remodeling, liver fibrosis, and renal interstitial injury, respectively.Medications such as SGLT2 inhibitors and GLP-1 receptor agonists may provide multi-organ protection by modulating macrophage activity. The current research presents several limitations, including species differences between humans and mice, ambiguous temporal transformation rules of macrophages, and inadequate specificity of targeted preparations.Future efforts should leverage spatial multi-omics and gene editing technologies to analyze the global regulatory network and develop highly selective targeted strategies. This approach can offer theoretical support for the integrated and precise prevention and management of metabolic comorbidities. - Source: PubMed
Publication date: 2026/09/18
Bai XiaofanBai JiangZhou Yun - Interferon regulatory factor 5 (IRF5) is genetically linked to ulcerative colitis (UC) susceptibility, yet its role in intestinal inflammation remains poorly understood. Here, we detected IRF5 expression in intestinal tissues from 29 UC patients and 10 healthy controls via immunohistochemistry and immunofluorescence. We constructed DSS-induced acute colitis models in IRF5-knockout (IRF5-/-) and wild-type (IRF5+/+) mice and analyzed the transcriptome of IRF5-knockdown macrophages. IRF5 was highly upregulated in inflamed intestinal tissues of UC patients and DSS-treated mice, primarily in CD68 macrophages. Compared with wild-type mice, IRF5-/- mice exhibited attenuated colitis, with reduced weight loss, lower disease activity index scores and milder colon shortening. Moreover, IRF5 deletion increased anti-inflammatory cytokines (IL-1rn, IL-10, IL-13, IL-17) and decreased pro-inflammatory cytokines (IL-1β, TNF). Transcriptome analysis revealed that IRF5 knockdown suppressed M1 pro-inflammatory genes (Ido1, Il12b) and upregulated the M2 marker MRC2. It also markedly inhibited TLR signaling and actin cytoskeleton regulation. Additionally, IRF5 downregulation reduced Tlr2 expression, indicating a positive feedback loop between IRF5 and TLR signaling. In summary, IRF5 exacerbates intestinal inflammation by promoting M1 macrophage polarization and activating TLR signaling, making it a promising therapeutic target for UC. - Source: PubMed
Publication date: 2026/09/17
Shao LimingChen YiWu LunpoZhong Jing - Parkinson's disease (PD) is associated with systemic inflammatory and metabolic alterations that may extend beyond the central nervous system. Although 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) reproduces several pathological features of Parkinsonian neurodegeneration, its effects on pancreatic tissue remain poorly characterized. This study investigated MPTP-associated pancreatic histopathological and immunohistochemical alterations and evaluated the potential attenuating effects of Hexarelin. Fifty male BALB/c mice were randomly assigned to five groups (n = 10/group): Sham, MPTP, Hexarelin, PreHexarelin, and PostHexarelin. Pancreatic tissues were examined using hematoxylin and eosin staining and immunohistochemistry for amylin, β-amyloid, caspase-3, glucagon, insulin, CD11b, CD68, interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α). MPTP administration was associated with marked pancreatic injury characterized by acinar degeneration, cytoplasmic vacuolization, vascular congestion, interstitial edema, inflammatory cell infiltration, and degeneration of the islets of Langerhans. Immunohistochemical analysis demonstrated increased inflammatory (CD11b, CD68, IL-1β, and TNF-α) and apoptosis-associated (caspase-3) marker immunoreactivity, together with increased β-amyloid immunoreactivity and decreased insulin and amylin immunoreactivities. Hexarelin treatment attenuated these histopathological and immunohistochemical alterations in both treatment groups, although the magnitude of improvement varied among individual markers. These findings suggest that MPTP exposure is associated with pancreatic inflammation, apoptosis-associated changes, and alterations in endocrine-marker immunoreactivity. Hexarelin treatment was associated with attenuation of these pathological changes and partial preservation of islet morphology and endocrine-marker immunoreactivity; however, the PostHexarelin findings should be interpreted cautiously because the absence of a sequence- and time-matched post-MPTP vehicle control prevents complete separation of Hexarelin-associated effects from temporal changes after MPTP administration. - Source: PubMed
Publication date: 2026/09/18
Şahin MeldaTopsakal ŞenayElmas OnurÖzmen Özlem - Severe obesity is linked to metabolic dysfunction-associated steatotic liver disease (MASLD), which can progress to metabolic dysfunction-associated steatohepatitis (MASH) and advanced fibrosis. Currently, there are no accurate tissue biomarkers for measuring immune-mediated liver injury or remission post-bariatric surgery. This study utilized digital pathology and immunohistochemistry to analyze liver biopsies from three patient groups: those with severe obesity and liver damage before bariatric surgery, their paired re-do biopsies post-surgery, and patients with severe obesity and without evaluable liver injury per NASH CRN criteria. Quantitative metrics assessed immune cell proportions and staining areas from whole-slide images. Following bariatric surgery, patients experienced a significant reduction in body mass index (BMI) and improvements in liver histology, although lobular inflammation persisted at a median follow-up of six years. Analysis of the innate immune response showed a notable increase in CD15 neutrophils postoperatively, along with a progressive accumulation of CD56 natural killer cells across healthy and pre- and post-surgical cohorts. Additionally, long-term post-surgical samples exhibited higher densities of CD68 and CD163 macrophages. Within the adaptive immune compartment, the number of CD4 T cells significantly increased after surgery, while the abundance of CD8 T cells remained stable across all groups. Overall, the livers of postsurgical patients displayed the highest burden of immune cells and a restructured hierarchy of immune populations. This indicates the presence of a unique immune microenvironment associated with surgery rather than a return to a "healthy liver" profile. Despite metabolic and histological improvements post-surgery, persistent immune activation suggests a unique immunological state where immune cells may play dual roles in both liver damage and repair, emphasizing the need for comprehensive immune profiling and targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/09/03
Onoiu Alina-IulianaGonzález-Serrano SergioCambra-Cortés VicenteJiménez-Franco AndreaGuilarte CarmenPeña Karla BeatrizRiu FrancescCamps JordiJoven JorgeParada David