IndraLab

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Hydroxychloroquine decreases the amount of TNF. 15 / 15
1 | 14

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"Administration of hydroxychloroquine (HCQ), a small molecule inhibitor of TLR7/8/9, following injury reduced NET formation, IL-10, and TNFalpha levels and ultimately mitigated muscle fibrosis and improved myofiber regeneration following IR injury."

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"HCQ was reported to inhibit the release of IL-6, IL-1β and TNF-α (108–110)."

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"Furthermore, HCQ treatment significantly inhibited renal interstitial infiltration of CD3 T cells and F4/80 macrophages (Fig. 1E–G), as well as the renal expression of the proinflammatory cytokines IL-1β and TNF-α (Fig. 1N, O)."
| PMC

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"Additionally, in a monocytic cell line, hydroxychloroquine attenuated TNF-alpha and IL6 expression in response to IL-1beta and TNF-alpha stimulation, respectively 46."

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"In contrast to lopinavir and ritonavir, chloroquine and hydroxychloroquine + azithromycin downregulated the expression of TNF and IL6."

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"Animal experiments [XREF_BIBR] indicate that HCQ can obviously downregulate the expression of interleukin 1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) in local submandibular gland of nonobese diabetic (NOD) mice on the levels of gene transcription and protein synthesis."

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"By deacidifying endolysosomes and Golgi, CQ and HCQ could reduce the secretion of, for example, the proinflammatory cytokines TNF-α, IL-1β and IL-6 [98,170]."

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"HCQ was reported to inhibit the release of IL-6, IL-1β and TNF-α (108) (109) (110) ."

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"HCQ significantly reduced the LPS-induced mRNA levels of the proinflammatory cytokines TNF-α (p < 0.05 or 0.01, Fig. 6b ) that was consisted with the previous study [28] , and HCQ reduced IL-1β (all p < 0.001, Fig. 6c ) in a dose-dependent manner."

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"In another single-arm study, administration of hydroxychloroquine to HIV infected persons who experienced suboptimal CD4 T-cell gains after highly active antiretroviral therapy (HAART) resulted in decreased levels of T-cell activation and decreased levels of inflammatory cytokines IL-6 and TNF in plasma."

No evidence text available

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"By deacidifying endolysosomes and Golgi, CQ and HCQ could reduce the secretion of, for example, the proinflammatory cytokine TNF-α, IL-1β and IL-6."

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"The protein levels of the proinflammatory cytokines iNOS and TNF-α were significantly increased after TBI (p < 0.05, Fig. 2a, b and p< 0.01, Fig. 2a, c) , while HCQ administration significantly reduced the levels of iNOS (p < 0.01, Fig. 2a, b) and TNF-α (p < 0.05, Fig. 2a, c) ."

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"Among the 51 patients enrolled in the study, HCQ treatment led to significantly reduced serum levels of TNF-α, IL-6, IL-8, VEGF-A, IL-1ra, and IL-2 (p < 0.0001; p = 0.0006; p = 0.0460, p = 0.0177; p < 0.0001; p = 0.0282, respectively) and to decreased (but not significantly) levels of MIP-1α (p = 0.0746)."

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"Tang et al. [25] found that HCQ inhibited the expression levels of IL-1β, IL-6, and TNF-α to protect against ischemia/reperfusion (I/R)-induced renal injury, which is consistent with our observations."