Inhibitory Action of Tetrandrine on Macrophage Production of Interleukin-1 (IL-l)-Like Activity and Thymocyte Proliferation

Kang, Ji-Hee; Lewis, Daniel M.; Castranova, Vincent; Rojanasakul, Yon; Banks, Daniel E.; C., J. Y.; H., J. K.

doi:10.3109/01902149209031703

Cited by 41 publications

(14 citation statements)

References 22 publications

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“…The interleukin-1 (IL-1) activity of BAL cell-conditioned media was determined according to a previously described method (Kang et al, 1992;Ma et al, 1999). Thymocytes were obtained from male CD-1 mice (6-10 wk of age) and suspended in RPMI-1640 medium supplemented with 2 mM glutamine, 100 U/ml penicillin, 100 µg/ml streptomycin, 10% heatinactivated fetal bovine serum, and 2 × 10 -5 M mercaptoethanol.…”

Section: Il-1 Determinationmentioning

confidence: 99%

TIME COURSE OF PULMONARY RESPONSE OF RATS TO INHALATION OF CRYSTALLINE SILICA: NF-kappa B ACTIVATION, INFLAMMATION, CYTOKINE PRODUCTION, AND DAMAGE

Porter

et al. 2002

Inhalation Toxicology

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In vitro studies suggest that silica-induced lung disease may be linked to processes regulated by nuclear factor-kappa B (NF-kappa B) activation, but this has not been examined in vivo. Rats were exposed to a silica aerosol of 15 mg/m(3) (6 h/day, 5 days/wk) for 116 days, and bronchoalveolar lavage (BAL) was conducted at various times during the exposure. Silica-induced pulmonary inflammation and damage were determined by measuring BAL cell differentials and first BAL fluid lactate dehydrogenase (LDH) activity and serum albumin concentrations, respectively. NF-kappa B activation and production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) by BAL cells were also measured. The results demonstrate that NF-kappa B activation occurred after 5 days exposure, and continued to increase thereafter. BAL cell production of IL-1 and TNF-alpha had increased incrementally by 10 and 30 days of exposure, respectively. This elevation continued through 79 days of exposure before further increasing at 116 days of exposure. Pulmonary inflammation and damage in silica-exposed rats were also significantly elevated at 5 days of exposure, further increased at a slow rate through 41 days of exposure, and dramatically increased thereafter. Taken together, the results indicate that the initial molecular response of NF-kappa B activation in BAL cells occurs in response to low levels of silica deposition in the lung and increases more rapidly versus exposure duration than silica-induced pulmonary inflammation, cellular damage, and cytokine production by BAL cells. This suggests that NF-kappa B activation in BAL cells may play an important role in the initiation and progression of silica-induced pulmonary inflammation, cellular damage, and fibrosis.

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Section: Il-1 Determinationmentioning

confidence: 99%

TIME COURSE OF PULMONARY RESPONSE OF RATS TO INHALATION OF CRYSTALLINE SILICA: NF-kappa B ACTIVATION, INFLAMMATION, CYTOKINE PRODUCTION, AND DAMAGE

Porter

et al. 2002

Inhalation Toxicology

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“…Tet has been shown to suppress the production and activity of human monocyte IL-1 in vitro (10)(11)(12). It is hypothesized that the ocular anti-inflammatory action of Tet may be related to the inhibition of IL-1.…”

mentioning

confidence: 99%

Tetrandrine Inhibits Breakdown of Blood-Aqueous Barrier Induced by Endotoxin and Interleukin-1α in Rats

Xiao¹,

Chiou²

1996

Journal of Ocular Pharmacology and Therapeutics

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Tetrandrine was shown to significantly inhibit uveitis induced by endotoxin and interleukin-1 alpha (IL-1 alpha) in rats. The dose-response curve of IL-1 alpha-induced uveitis was inhibited in a non-competitive manner. The maximum inflammation induced by IL-1 alpha was suppressed to 58.4%, 38.3% and 18.3% of the control peak by 5 mg/kg, 10 mg/kg and 20 mg/kg t.i.d. of tetrandrine, respectively. The maximum inflammation induced by endotoxin was suppressed to 56.5% and 38.0% by 5 mg/kg and 10 mg/kg t.i.d. of tetrandrine, respectively. The mechanism of tetrandrine's anti-inflammation could involve numerous pathways of inflammation processes and multiple inflammatory mediators. The results of this study indicate that tetrandrine appears to be a broad spectrum, non-steroidal, novel ocular anti-inflammatory agent.

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“…Many iNOS inhibitors have been reported to be beneficial in endotoxemic conditions. Previously, we reported that isoquinoline analogs inhibit iNOS mRNA and protein expression in rat aorta and RAW 264.7 cells, induced by LPS and cytokines (Tainlin et al, 1982;Kang et al, 1992;Chen et al, 1997). Therefore, isoquinoline alkaloids are of special interest for their pharmacological actions on inflammation and related disorders.…”

mentioning

confidence: 99%

Regulation of Lipopolysaccharide-Induced Inducible Nitric-Oxide Synthase Expression through the Nuclear Factor-κB Pathway and Interferon-β/Tyrosine Kinase 2/Janus Tyrosine Kinase 2-Signal Transducer and Activator of Transcription-1 Signaling Cascades by 2-Naphthylethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (THI 53), a New Synthetic Isoquinoline Alkaloid

Kim

Tsoyi²,

Heo³

et al. 2006

J Pharmacol Exp Ther

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The effects of 2-naphthylethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (THI 53), on nitric oxide (NO) production and inducible nitric-oxide synthase (iNOS) protein induction by lipopolysaccharide (LPS) were investigated in RAW 264.7 cells and mice. In cells, THI 53 concentration dependently reduced NO production and iNOS protein induction by LPS. In addition, THI 53 inhibited NO production and iNOS protein induction in LPS-treated mice. LPS-mediated iNOS protein induction was inhibited significantly by the specific tyrosine kinase inhibitor ␣-cyano-(3-hydroxy-4-nitro)cinnamonitrile (AG126) as well as by THI 53. In addition, a c-Jun NH 2 -terminal kinase (JNK) inhibitor anthra[1,9-cd]pyrazole-6 (2H)-one) (SP600125) but not an extracellular regulated kinase inhibitor [2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98029)] or a p38 inhibitor [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB230580)] reduced the iNOS protein level induced by LPS. Moreover, a Janus kinase 2 (JAK2) inhibitor ␣-cyano-(3,4-dihydroxy)-N-benzylcinnamide (AG490) dose-dependently prevented LPS-mediated iNOS protein induction. LPS activated phosphorylations of tyrosine kinases, especially tyrosine kinase 2 (Tyk2) and signal transducer and activator of transcription-1 (STAT-1); these were reduced by THI 53. LPS also phosphorylated the JNK pathway; however, this phosphorylation was unaffected by THI 53. Interestingly, a JNK inhibitor (SP600125) and another tyrosine kinase inhibitor (genistein) significantly inhibited STAT-1 phosphorylation, suggesting that the LPS-activated JNK pathway and a tyrosine kinase pathway (especially Tyk2) may link to the STAT-1 pathway, which is involved in iNOS induction. However, THI 53 regulates LPS-mediated iNOS protein induction by affecting the Tyk2/JAK2-STAT-1 pathway, not the JNK pathway. The inhibition by THI 53 of LPS-induced NO production was recovered by a tyrosine phosphatase inhibitor (Na 3 VO 4 ), which supports the possibility that THI 53 inhibits the LPS-induced inflammatory response through regulation of tyrosine kinase pathways. THI 53 also inhibited LPS-mediated interferon (IFN)-␤ production and nuclear factor-B (NF-B) activation. Thus, THI 53 may regulate LPS-mediated inflammatory response through both the NF-B and IFN-␤/Tyk2/JAK2-STAT-1 pathways.The expression of inducible nitric-oxide synthase (iNOS) and the production of large quantities of nitric oxide (NO) may contribute to the pathophysiology of endotoxemia or sepsis (Thiemermann and Vane, 1990). Moreover, mice carrying the null mutant gene for iNOS are resistant to the hypotension and death caused by lipopolysaccharide (LPS) This study was supported by the Korea Science and Engineering Foundation (R13-2005-005-01003-0).H.J.K. and K.T. contributed equally to this work.

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Inhibitory Action of Tetrandrine on Macrophage Production of Interleukin-1 (IL-l)-Like Activity and Thymocyte Proliferation

Cited by 41 publications

References 22 publications

TIME COURSE OF PULMONARY RESPONSE OF RATS TO INHALATION OF CRYSTALLINE SILICA: NF-kappa B ACTIVATION, INFLAMMATION, CYTOKINE PRODUCTION, AND DAMAGE

TIME COURSE OF PULMONARY RESPONSE OF RATS TO INHALATION OF CRYSTALLINE SILICA: NF-kappa B ACTIVATION, INFLAMMATION, CYTOKINE PRODUCTION, AND DAMAGE

Tetrandrine Inhibits Breakdown of Blood-Aqueous Barrier Induced by Endotoxin and Interleukin-1α in Rats

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