Effects of a dual inhibitor of tumor necrosis factor-α and interleukin-1 on lipopolysaccharide-induced lung injury in rats: Involvement of the p38 mitogen-activated protein kinase pathway

Yoshinari, Daisuke; Takeyoshi, Izumi; Koibuchi, Yukio; Matsumoto, Koshi; Kawashima, Yasunaru; Koyama, Toru; Ohwada, Susumu; Morishita, Yasuo

doi:10.1097/00003246-200103000-00029

Cited by 79 publications

(43 citation statements)

References 32 publications

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“…The samples were dried in a hot air oven at 80°C for 72 h. Later, the dried tissue was weighed. The wet-to-dry ratio was calculated with the following equation: ratio = wet weight/dry weight (Yoshinari, 2001). …”

Section: Determination Of Pulmonary Edemamentioning

confidence: 99%

The Effects ofPortulaca oleraceaon Hypoxia-Induced Pulmonary Edema in Mice

Yue

Wen

et al. 2015

High Altitude Medicine & Biology

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Tan Yue, Wen Xiaosa, Qi Ruirui, Shi Wencai, Xin Hailiang, and Li Min. The effects of Portulaca oleracea on hypoxia-induced pulmonary edema in mice. High Alt Med Biol 16:43-51, 2015-Portulaca oleracea L. (PO) is known as ''a vegetable for long life'' due to its antioxidant, anti-inflammatory, and other pharmacological activities. However, the protective activity of the ethanol extract of PO (EEPO) against hypoxia-induced pulmonary edema has not been fully investigated. In this study, we exposed mice to a simulated altitude of 7000 meters for 0, 3, 6, 9, and 12 h to observe changes in the water content and transvascular leakage of the mouse lung. It was found that transvascular leakage increased to the maximum in the mouse lung after 6 h exposure to hypobaric hypoxia. Prophylactic administration of EEPO before hypoxic exposure markedly reduced the transvascular leakage and oxidative stress, and inhibited the upregulation of NF-kB in the mouse lung, as compared with the control group. In addition, EEPO significantly reduced the levels of proinflammatory cytokines and cell adhesion molecules in the lungs of mice, as compared with the hypoxia group. Our results show that EEPO can reduce initial transvascular leakage and pulmonary edema under hypobaric hypoxia conditions.

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Section: Determination Of Pulmonary Edemamentioning

confidence: 99%

The Effects ofPortulaca oleraceaon Hypoxia-Induced Pulmonary Edema in Mice

Yue

Wen

et al. 2015

High Altitude Medicine & Biology

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“…On the other hand, FR167653 was first discovered as a potent inhibitor of tumor necrosis factor (TNF)-␣ and interleukin-1␤ production (Yamamoto et al, 1996(Yamamoto et al, , 1997. Recent reports have shown that FR167653 inhibits the activation of p38 MAPK by suppressing the phosphorylation of p38, preferentially in the ␣ isoform, but not in the ␥ isoform Takahashi et al, 2001;Yoshinari et al, 2001). We therefore investigated whether not only SB203580 but also FR167653 blocks the SNL-induced thermal hyperalgesia (Fig.…”

Section: Inhibition Of P38 Activation Attenuates L5 Snl-induced Thermmentioning

confidence: 99%

Role of Mitogen-Activated Protein Kinase Activation in Injured and Intact Primary Afferent Neurons for Mechanical and Heat Hypersensitivity after Spinal Nerve Ligation

Obata¹,

Yamanaka²,

Kobayashi³

et al. 2004

J. Neurosci.

290

208

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To investigate whether activation of mitogen-activated protein kinase (MAPK) in damaged and/or undamaged primary afferents participates in neuropathic pain after partial nerve injury, we examined the phosphorylation of extracellular signal-regulated protein kinase (ERK), p38 MAPK, and c-Jun N-terminal kinase (JNK) in the L4 and L5 dorsal root ganglion (DRG) in the L5 spinal nerve ligation (SNL) model. We first confirmed, using activating transcription factor 3 and neuropeptide Y immunoreactivity, that virtually all L4 DRG neurons are spared from axotomy in this model. In the injured L5 DRG, the L5 SNL induced the activation of ERK, p38, and JNK in different populations of DRG neurons. In contrast, in the uninjured L4 DRG, the L5 SNL induced only p38 activation in tyrosine kinase A-expressing small-to medium-diameter neurons. Intrathecal ERK, p38, and JNK inhibitor infusions reversed SNL-induced mechanical allodynia, whereas only p38 inhibitor application attenuated SNL-induced thermal hyperalgesia. Furthermore, the L5 dorsal rhizotomy did not prevent SNL-induced thermal hyperalgesia. We therefore hypothesized that p38 activation in the uninjured L4 DRG might be involved in the development of heat hypersensitivity in the L5 SNL model. In fact, the treatment of the p38 inhibitor and also anti-nerve growth factor reduced SNL-induced upregulation of brain-derived neurotrophic factor and transient receptor potential vanilloid type 1 expression in the L4 DRG. Together, our results demonstrate that the L5 SNL induces differential activation of MAPK in injured and uninjured DRG neurons and, furthermore, that MAPK activation in the primary afferents may participate in generating pain hypersensitivity after partial nerve injury.

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“…4 Activation of p38 MAPK can induce the production and secretion of proinflammatory cytokines such as interleukin-1␤ and tumor necrosis factor-␣ (TNF-␣). 5 In turn, interleukin-1␤ and TNF-␣ can activate p38 MAPK, which leads to autocrine and paracrine promotion of an inflammatory response that exacerbates kidney injury. 6,7 Increased activity of p38 MAPK has been observed in patients suffering from inflammatory bowel disease, human diabetic nephropathy, and glomerulonephritis.…”

mentioning

confidence: 99%

Inhibition of p38 Mitogen-Activated Protein Kinase and Transforming Growth Factor-β1/Smad Signaling Pathways Modulates the Development of Fibrosis in Adriamycin-Induced Nephropathy

Campanale

Liang

et al. 2006

The American Journal of Pathology

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Inflammation and fibrogenesis are the two determinants of the progression of renal fibrosis, the common pathway leading to end-stage renal disease. The p38 mitogen-activated protein kinase (MAPK) and transforming growth factor (TGF)-␤1/Smad signaling pathways play critical roles in inflammation and fibrogenesis, respectively. The present study examined the beneficial renoprotective effect of combination therapy using the p38 MAPK pathway inhibitor (SB203580) and a TGF-␤ receptor I (ALK5) inhibitor (ALK5I) in a mouse model of adriamycin (ADR) nephrosis. The p38 MAPK and TGF-␤1/Smad2 signaling pathways were activated in ADR-induced nephropathy in a sequential time course manner. Two weeks after ADR injection, the combined administration of SB203580 (1 mg/kg/24 hours) and ALK5I (1 mg/kg/24 hours) markedly reduced p38 MAPK and Smad2 activities. Moreover, the co-administration of SB203580 and ALK5I to ADR-injected mice resulted in a down-regulation of total and active TGF-␤1 production, reduced myofibroblast accumulation, and decreased expression of collagen type IV and fibronectin. In these mice, retardation in the development of glomerulosclerosis and interstitial fibrosis was observed. In conclusion, although p38 MAPK and TGF-␤1/Smad signaling pathways are distinct they coordinate the progression of renal fibrosis in ADR nephrosis. The co-administration of a p38 MAPK inhibitor and an ALK5 inhibitor may have potential applications in the treatment of renal fibrosis. (Am J Pathol 2006, 169

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Effects of a dual inhibitor of tumor necrosis factor-α and interleukin-1 on lipopolysaccharide-induced lung injury in rats: Involvement of the p38 mitogen-activated protein kinase pathway

Abstract: FR167653 administration decreased serum TNF-alpha and IL-1beta concentrations, which was associated with decreased lung injury and lethality. The mechanism responsible for the decreased TNF-alpha and IL-1 may be related to the inhibitory effect of FR167653 on p38 MAP kinase activation.

Cited by 79 publications

References 32 publications

The Effects ofPortulaca oleraceaon Hypoxia-Induced Pulmonary Edema in Mice

The Effects ofPortulaca oleraceaon Hypoxia-Induced Pulmonary Edema in Mice

Role of Mitogen-Activated Protein Kinase Activation in Injured and Intact Primary Afferent Neurons for Mechanical and Heat Hypersensitivity after Spinal Nerve Ligation

Inhibition of p38 Mitogen-Activated Protein Kinase and Transforming Growth Factor-β1/Smad Signaling Pathways Modulates the Development of Fibrosis in Adriamycin-Induced Nephropathy

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