Targeting HMGB1 in the treatment of sepsis

Wang, Haichao; Ward, M.F.; Sama, Andrew E.

doi:10.1517/14728222.2014.863876

Cited by 124 publications

(107 citation statements)

References 133 publications

(147 reference statements)

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“…However, caution should be exercised when using gene knockout approaches to evaluate the pathogenic roles of any particular mediators that are still critically needed for maintaining beneficial physiological functions. For instance, despite the well-established pathogenic role of HMGB1 in infection-and injuryelicited inflammatory diseases (60,61), the disruption of HMGB1 expression adversely renders animals more susceptible to infectious (62) or injurious insults (63,64), reinforcing the dramatically distinct roles of HMGB1 in health and disease (65). Similarly, in an animal model of dextran sodium sulfate (DSS)-induced colitis, SAA1/2 knockout mice appeared to be more susceptible to colitis, possibly because the intestinal epithelia-derived SAAs are still critically needed for bactericidal activities (34).…”

Section: Discussionmentioning

confidence: 99%

Serum Amyloid A Stimulates PKR Expression and HMGB1 Release Possibly through TLR4/RAGE Receptors

Zhu

et al. 2015

Mol Med

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Section: Discussionmentioning

confidence: 99%

Serum Amyloid A Stimulates PKR Expression and HMGB1 Release Possibly through TLR4/RAGE Receptors

Zhu

et al. 2015

Mol Med

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“…Our present results demonstrated that NCPB treatment can reduce the concentrations of proinflammatory cytokines, including TNF-α, IL-1β and IL-6, which indicated that NCPB can alleviate the function damages of liver and kidney after PH. HMGB1 is an important late inflammatory medium, and plays a crucial role in delayed lethal effect of sepsis [20,21]. In our investigation, NCPB can down-regulate the expression of HMGB1 obviously.…”

Section: Discussionmentioning

confidence: 58%

Ameliorative Effects of Neurolytic Celiac Plexus Block on Stress and Inflammation in Rats with Partial Hepatectomy

Li¹,

Li²,

X.³

et al. 2015

Trop. J. Pharm Res

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Purpose: To investigate effects of neurolytic celiac plexus block (NCPB) on stress and inflammation in rats with partial hepatectomy (PH). Methods: A model of PH rat was established, and serum C-reactive protein (CRP); corticosterone (GC); adrenocorticotropin (ACTH); noradrenaline (NA); adrenalin (AD); aspartate transaminase (AST); alanine transaminase (ALT); as well as tumor necrosis factor-α (TNF-α); interleukin (IL)-1β and IL-6; high mobility group box1 (HMGB1); and nitric oxide (NO) concentrations in serum assessed after PH. Additionally, Western blotting was performed to determine the effect of NCPB on expressions of glucocorticoid receptors (GR), inhibitor of nuclear factor kappa B (IκB), p65, c-Jun and inducible nitric oxide synthase (iNOS) of PH rats, as well as assay effects of NCPB on nuclear translocation of GR, cJun and p65. DNA binding activities of nuclear factor kappa B (NF-κB) and activator protein 1 (AP-1) were also determined. Results: NCPB reduced AST and ALT (P < 0.05), decreased secretion of inflammatory cytokines and NO (P < 0.05), as well as decreased CRP, GC, ACTH, NA and AD after PH (p < 0.05). NCPB increased expressions of GR and IκB, but expressions of p65, and iNOS (p < 0.05

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“…This was observed in the patients in the control group in the present study, however, the serum levels of IFN-γ did not change significantly in the patients in the lidocaine group, which maintained the balance of Th1/Th2. HMGB1, as a critical mediator of several inflammatory diseases, is important in surgery-associated sepsis (22). It is also implicated in non-inflammatory conditions, including cancer, by regulating tumorigenesis and contributing to metastasis (23).…”

Section: Discussionmentioning

confidence: 99%

Intraoperative intravenous lidocaine exerts a protective effect on cell-mediated immunity in patients undergoing radical hysterectomy

Wang

Yan

Liu

et al. 2015

Molecular Medicine Reports

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Abstract. Surgical procedures cause a decrease in lymphocyte proliferation rate, an increase in apoptosis and shifts the balance of T-helper (Th)1/Th2 cells towards anti-cell-mediated immunity (CMI) Th2 dominance, which is relevant to the immunosuppressive effects of CMI, postoperative septic complications and the formation of tumor metastasis. Previous studies have revealed that lidocaine exhibits antibacterial actions; regulating inflammatory responses, reducing postoperative pain and affecting the duration spent in hospital. Thus, the present study hypothesized that lidocaine may exert a protective effect on the CMI of patients undergoing surgery for the removal of a primary tumor. A total of 30 adult female patients diagnosed with cervical cancer were recruited to the present study and were randomized into two groups. The lidocaine group received an intravenous bolus dose of 1.5 mg/kg lidocaine, followed by continuous infusion at 1.5 mg/kg/h until discharge from the operating room. The control group received the same volume of normal saline. A 10 ml sample of venous blood was drawn, and the lymphocytes were isolated using Ficoll-paque 1 day prior to surgery, at discharge from the operating room and 48 h post-surgery. The proliferation rate of the lymphocytes was assessed using a Cell Counting Kit-8 assay and was found to be higher in the lidocaine group. The early apoptosis of lymphocytes was attenuated following lidocaine treatment at 48 h post-surgery, as detected using flow cytometry with Annexin V-fluorescein isothiocyanate/propidium iodide staining. The level of interferon (IFN)-γ in the serum at 48 h was significantly decreased following surgery in the control group, compared with the pre-surgical values (3.782±0.282, vs. 4.089±0.339 pg/ml, respectively) and the ratio of IFN-γ to interleukin-4 was well preserved in the lidocaine group. In conclusion, the present study demonstrated that the intraoperative systemic administration of lidocaine exerted a protective effect on CMI in patients with cervical cancer undergoing radical hysterectomy. This may be beneficial in reducing the occurrence of postoperative septic complications and tumor metastasis formation.

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Targeting HMGB1 in the treatment of sepsis

Cited by 124 publications

References 133 publications

Serum Amyloid A Stimulates PKR Expression and HMGB1 Release Possibly through TLR4/RAGE Receptors

Serum Amyloid A Stimulates PKR Expression and HMGB1 Release Possibly through TLR4/RAGE Receptors

Ameliorative Effects of Neurolytic Celiac Plexus Block on Stress and Inflammation in Rats with Partial Hepatectomy

Intraoperative intravenous lidocaine exerts a protective effect on cell-mediated immunity in patients undergoing radical hysterectomy

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