IL1B (Interleukin 1, beta)

CD146+ hPDL-MSCs do not always show higher levels of immunomediator expression. Further research is necessary to isolate hPDL-MSC subpopulations with optimal potential for therapeutic applications.

These findings evidence the notion that the sigma-1 receptor may be a promising therapeutic target for ischemic injury. Abbreviations: aCSF, artificial cerebrospinal fluid; AD, anoxic depolarization; Cornu Ammonis 1, CA1; ER, endoplasmic reticulum; fEPSP, field excitatory postsynaptic potentials; GRP78, 78-kDa glucose-regulated protein; GRP94, glucose-regulated protein 94; IL-1β, interleukin-1 beta; MAMs, mitochondria-associated membranes; MMP-9, matrix metalloproteinase-9; OGD, oxygen and glucose deprivation; PI, propidium iodide; p-NF-κB, phosphorilated nuclear factor -kappa-B p65 subunit (p-p65); ROS, reactive oxygen species; Sig-1 receptor, sigma-1 receptor; TNF-α, tumor necrosis factor-alpha; UPR, unfolded protein response.

TP intervention mitigated alterations in brain structure and function as well as anxiety and depression-like behaviors in aged T2DM rats.

Concomitantly, NBIF also reduces levels of pro-inflammatory cytokines IL-1β, TNF-α, and IL-6, thereby attenuating DSS-induced pathological damage in UC. This study not only proposes a novel anti-senescence strategy for UC treatment but also elucidates the pivotal role of the gut microbiota-metabolite-AMPK axis in regulating intestinal inflammation.

Collectively, we show OLs as an unrecognized source of HMGB1 during oxycodone exposure and establish a novel OL-microglia signaling axis underlying neuroinflammation. These insights emphasize the importance of glial crosstalk in opioid-related pathologies and may inform therapeutic strategies targeting HMGB1 signaling.

In addition, our in vitro system allowed functional assessment of PDO-exposed monocytes demonstrating a compromised capacity to mount an inflammatory response upon TLR stimulation. Together, PDO-monocyte co-cultures offer a platform to dissect the interplay between cancer cells and monocytes, and advance our understanding of myeloid plasticity and function in cancer patients.

BXD intervention demonstrated significant therapeutic effects in GPL mice. The underlying mechanisms are associated with the restoration of gastric microbiota dysbiosis, promotion of beneficial bacterial growth, suppression of potential pathogens, modulation of the inflammatory response, and alleviation of mucosal damage.

Finally, our translational pathway should be prioritized with orthogonal confirmation, interference testing, and clinically meaningful reporting to be adopted in the field of laboratory medicine. This supports reproducible biomarkers for clinical decision-making.

Moreover, 6-OHDA induces distinct inflammatory responses depending on the stage of oligodendrocyte differentiation. These findings highlight the dual role of oligodendrocytes as both iron reservoirs and modulators of the neuroinflammatory microenvironment, providing new insights into the cellular mechanisms underlying nigral iron accumulation in PD, and suggesting that oligodendrocytes play a critical regulatory role in PD pathogenesis.

Furthermore, CUR@HA-C60 demonstrated favorable biosafety profiles in murine models and significantly improved CUR bioavailability by suppressing inflammation, reducing OS-related damage, and restoring intestinal epithelial integrity. These findings indicate that CUR@HA-C60 represents a promising oral therapeutic strategy for the treatment of inflammatory diseases.

These findings suggest that placental sEVs play a critical role in modulating astrocyte responses to oxidative stress and mitochondrial dysfunction. The ability of sEVs to restore redox homeostasis highlights their potential physiological function in fetal neuroprotection against environmental stressors.

The combination of KPT-8602 and IFN-γ can activate the pan-apoptotic pathway by upregulating ZBP1, thereby effectively inhibiting the growth of PCNSL. This study presented a promising new combination treatment strategy for PCNSL.