rR TNF-alpha
- Known as:
- rR TNF-a
- Catalog number:
- AK8320-1000
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Akro
- Gene target:
- TNF-alpha
Related products to: rR TNF-alpha
Related articles to: rR TNF-alpha
- The expression of certain miRNAs are significantly associated with both inflammatory and ischemia-reperfusion (I/R) injury in ischemic stroke. In this study, we identified cerebral cortex miR-125a-5p via RNA sequencing, which showed significant enrichment in inflammatory pathways. Cerebral infarction volume and neurological deficits were evaluated using TTC staining, mNSS scoring, and the open field test. Nissl staining and TUNEL assays were used to assess cortical apoptosis. TRAF2, NIK, and p-NFκB levels in the cerebral cortex, as well as serum TNF-α, IL-1β, and IFN-γ concentrations, were measured by Western blot and ELISA. We found that TRAF2, a predicted target of miR-125a-5p, is linked to NF-κB pathway. Overexpression of miR-125a-5p reduced infarct volume, inhibited apoptosis and neurological deficits, and downregulate TRAF2, NIK and p-NF-κB in the cortex, along with TNF-α, IL-1β, and INF-γ in the serum of I/R rats. The miR-125a-5p negatively regulates TRAF2, alleviating inflammation-induced I/R injury by modulating the NF-κB pathway. - Source: PubMed
Publication date: 2026/09/21
Niu ShouruiGuo ChujiaZhang JinfenLi ChunyanZhu HengLiao HongyuYang JinweiMa WeiLi Liyan - Chronic spontaneous urticaria (CSU) includes 2 autoimmune endotypes, type I (autoallergic) and type IIb (autoimmune), which differ in pathogenesis and treatment response. However, practical criteria for distinguishing these endotypes in routine clinical practice remain limited. - Source: PubMed
Publication date: 2026/09/24
Ji JiangChen LuMa NiYao YuxuZhang ChuqiaoLi EnzeJiao Qingqing - Diabetic peripheral neuropathy (DPN) is a prevalent and disabling complication, with over 50% of diabetic patients affected. Current pharmacologic therapies are limited by adverse effects, highlighting the need for safer alternatives. Preliminary evidence suggests that low-frequency (2 Hz) electroacupuncture (EA) may be beneficial, but high-quality clinical trials investigating its mechanisms are lacking. - Source: PubMed
Publication date: 2026/09/30
Chen NisangLi RongrongLuo Ning - Childhood peer abuse is a developmentally salient form of interpersonal adversity, yet its role in shaping links between peripheral biological stress markers and brain structure remains poorly understood. The present cross-sectional study examined whether retrospectively reported childhood peer verbal and physical abuse moderated associations of systemic inflammatory burden and hair cortisol with subcortical brain volume. Participants from a community sample completed the Maltreatment and Abuse Chronology of Exposure scale and structural magnetic resonance imaging. Inflammatory burden was indexed by a composite of standardised IL-6, IL-8, TNF-alpha, and C-reactive protein values ( = 292), and hair cortisol was available in a subsample ( = 172). Bilateral amygdala, hippocampus, putamen, and caudate volumes were extracted from FreeSurfer segmentation. Linear regression models adjusted for gender, age, parental education, and estimated total intracranial volume; false discovery rate correction was applied across the four ROI tests within each marker-by-moderator family. Peer verbal abuse moderated associations of inflammatory burden with bilateral amygdala volume ( = -.095, pFDR = .032) and bilateral putamen volume ( = -.115, pFDR = .017). Peer physical abuse moderated the association between hair cortisol and bilateral amygdala volume ( = .227, pFDR = .035). Caudate models did not survive correction. Core findings remained significant after sensitivity adjustment for broader childhood adversity and current depression/anxiety symptoms. Associations differed across brain regions, biological markers, and peer-abuse subtypes. These findings identify peer adversity as an important interpersonal context for understanding stress-related brain differences. - Source: PubMed
Publication date: 2026/10/05
Bu LaijunWang Zhen - Beyond its primary lipid-lowering efficacy, simvastatin (SIM) demonstrates neuroprotective potential mediated by its antioxidant, anti-apoptotic, and anti-inflammatory bioactivities. Consequently, the current study tested the hypothesis that SIM confers neuroprotection in a rodent model of depressive-like phenotypes induced by Doxorubicin (DOX)/Cyclophosphamide (CP) polychemotherapy. Rats were divided into four cohorts (n = 10 per group). Control; SIM-alone; chemotherapy; SIM/chemotherapy combination. SIM co-treatment significantly improved depression-like phenotypes throughout the forced swim test, the sucrose splash test as well as the open field test. This is in addition to alleviating hippocampal neuro-inflammation and oxidative stress vs the chemotherapy-combination group. Concurrently, SIM reduced hippocampal oxidative stress (51% decrease in MDA) and inflammation (70% and 42% decrease in TNF-α and NF-κB). SIM also attenuated apoptosis (29% reduction in active caspase-3). Pathway enrichment (PEA) and Gene Ontology (GO) analyses supported that SIM's cytoprotective effects may be mediated through multiple pathways, including lipid metabolism, immunity, and apoptosis regulation. In conclusion, SIM co-administration effectively attenuated the molecular alterations elicited by the DOX/CP combination within the hippocampal tissues. Collectively, these data position SIM as a promising candidate for mitigating chemotherapy-associated depression. Nevertheless, further investigation is warranted to fully elucidate the underlying antidepressant mechanisms of statins and to validate their clinical efficacy. - Source: PubMed
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