Compared with minocycline hydrochloride alone, the addition of tinidazole further improved patients' periodontal health, reduced the inflammatory response and MMP-9, SIgA levels, and did not increase the risk of adverse reactions. This suggests good drug safety and clinical promotion value.
Finally, molecular docking results showed B-cell CLL/lymphoma 2 (BCL2-6), CTNNB1, HSP90AA1, plasminogen activator urokinase (PLAU), and α protein kinase C alpha (PRCAKA) bound to minocycline better. This article concluded that minocycline was effective in treating SCI by improving neurological recovery and inhibiting oxidative stress, apoptosis, and inflammation.
1 month ago
Clinical • Retrospective data • Journal
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EGFR (Epidermal growth factor receptor) • BCL2 (B-cell CLL/lymphoma 2) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • CTNNA1 (Catenin Alpha 1) • PRKCA (Protein Kinase C Alpha) • HSP90AA1 (Heat Shock Protein 90 Alpha Family Class A Member 1Heat Shock Protein 90 Alpha Family Class A Member 1)
Adult male mice were treated with the chemotherapeutic drugs 5-fluorouracil and leucovorin (5-Fu/LV, intraperitoneal injection, I.P.) on Days 1, 8, and 15 at a dosage of 50 mg/kg for 5-Fu and 90 mg/kg for LV for 3 weeks...Furthermore, 5-Fu/LV treatment reduced the long-term potentiation (LTP) recorded in the hippocampal CA1 region in response to a theta burst stimulation of the CA3-CA1 pathway and decreased the evoked N-methyl-D-aspartic acid receptor (NMDAR)-excitatory postsynaptic currents (NMDAR-EPSCs) in CA1 neurons. Cotreatment with the microglial inhibitor minocycline (33 mg/kg, daily for 3 weeks) restored cognitive deficits and microglial ramification, decreased the number of CD68-positive microglia, and reversed the reductions in LTP and the amplitude of NMDAR-EPSCs in 5-Fu/LV-treated mice. Our data suggest that microglial dysfunction and related synaptic dysfunction contribute to 5-Fu/LV-induced cognitive impairment.
The conditioned medium from sevoflurane-treated microglia inhibited the OPC proliferation and differentiation, while minocycline or PLX5622 alleviated sevoflurane-induced neuroinflammation and hypomyelination. Therefore, repeated sevoflurane exposure negatively affected OPC differentiation and myelination trajectory through hyperactivating microglia in developing brain, leading to motor and cognitive impairments, while microglial inhibition/depletion could protect against sevoflurane-induced damage on developing myelination.
Therapies for ENL management, such as thalidomide, methotrexate, apremilast, minocycline and tumour necrosis factor-alpha inhibitors, hold potential. This review addresses recent advances in leprosy reaction pathogenesis and diagnostics, offering therapeutic insights and preventive strategies to mitigate their onset.
We evaluated whether higher plasma interleukin 6 (IL-6) levels would be associated with more severe negative or depressive symptoms in schizophrenia and explored illness stage utilizing early (BeneMin [Benefit of Minocycline on Negative Symptoms of Psychosis: Extent and Mechanism], n = 201, 72.8% male) and established (iRELATE [Immune Response & Social Cognition in Schizophrenia], n = 94, 67.3% male) schizophrenia cohorts...All analyses were adjusted for sex, age, and chlorpromazine equivalent dose...Our results indicate that higher plasma IL-6 levels may be differently associated with the severity of depressive and negative symptoms dependent on the illness stage. Future work identifying elevated levels of inflammation in larger samples may allow stratification and personalized intervention by subgroups who are at risk of poor outcomes.
Moreover, it was found that the TLR4/MyD88/NF-κB pathway was involved in the shift of microglia from a pro-inflammatory (M1) to an anti-inflammatory (M2). In summary, minocycline likely mediated the process of microglia polarization partly via the TLR4/MyD88/NF-κB pathway, promoting neuronal survival and restoring synaptic plasticity, thereby improving TN-related cognitive impairment.
P1, N=30, Not yet recruiting, University of Cincinnati | Trial completion date: Jun 2026 --> Dec 2026 | Trial primary completion date: Dec 2025 --> May 2026
5 months ago
Trial completion date • Trial primary completion date
P2, N=15, Recruiting, Radboud University Medical Center | Trial completion date: Sep 2024 --> Dec 2025 | Trial primary completion date: Aug 2024 --> Aug 2025
5 months ago
Trial completion date • Trial primary completion date • Nontuberculous mycobacteria
Clinically used drugs deferiprone and minocycline reduced mitochondrial iron and superoxide levels, resulting in decreased colon tumor cell growth in vitro and in vivo. Manipulating the mitochondrial iron uptake protein MCU (mitochondrial calcium uniporter) also affected cell and xenograft tumor growth. This study suggests that therapies aimed at reducing mitochondrial iron levels may effectively inhibit colon tumor growth, particularly in patients with low PINK1 expression.
In mice with pancreatic cancer-induced pain, the microglia activation in the NTS was observed, characterized by increased cell density and decreased process number and length, while injection of microglia inhibitor minocycline in the NTS alleviated pancreatic cancer-induced pain...Blocking CXCL1-CXCR2 signaling by injection of CXCL1 neutralizing antibody or CXCR2 antagonist SB225002 in the NTS of mice with pancreatic cancer-induced pain alleviated abdominal hypersensitivity and hunching behavior, and also reversed the activation of neurons and microglia. Additionally, injection of recombinant CXCL1 in the NTS of sham-operated mice induced abdominal pain, and activated the neurons and microglia. In summary, our study highlights the critical role of NTS microglia activation mediated by CXCL1-CXCR2 signaling in pancreatic cancer-induced pain.
P4, N=574, Not yet recruiting, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology; Tongji Hospital, Tongji Medical College, Huazhong University o
This indicates that ciprofloxacin enhances autophagy, increasing the amount of free Beclin-1 via phosphorylated Bcl-2, and inhibits caspase activity. Therefore, ciprofloxacin might protect against renal tubular injury through the activation of autophagy in the setting of acute kidney injury.
Inhibition of microglia by pretreatment with minocycline or depletion of microglia by PLX3397 abolished the preventive effect of low-dose LPS pre-injection on mSPS-induced anxiety- and fear-like behavior and neuroinflammatory responses. These results suggest that pre-stimulation of microglia may prevent the development of PTSD-like behaviors by attenuating the development of neuroinflammatory responses. This could help to develop new strategies to prevent the damaging effects of harmful stress on the brain.