Diterpenoid trigonoreidon B isolated from Trigonostemon reidioides alleviates inflammation in models of LPS-stimulated murine macrophages and inflammatory liver injury in mice

Utaipan, Tanyarath; Suksamrarn, Apichart; Kaemchantuek, Praphakorn; Chokchaisiri, Ratchanaporn; Stremmel, Wolfgang; Chamulitrat, Waleé; Chunglok, Warangkana

doi:10.1016/j.biopha.2018.02.144

Cited by 18 publications

(12 citation statements)

References 40 publications

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“…Elicitation of inflammation response plays a crucial role in the pathological process of CCl 4 -induced liver injury [52,53]. Previous studies have shown that the expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and inflammatory mediators (COX-2 and iNOS) plays important role in the development and maintenance of inflammation related to liver injury [19,[54][55][56]. iNOS is responsible for the production NO, which is a highly reactive molecule synthesized from L-arginine.…”

Section: Discussionmentioning

confidence: 99%

Indole-3-Carbinol Derivative DIM Mitigates Carbon Tetrachloride-Induced Acute Liver Injury in Mice by Inhibiting Inflammatory Response, Apoptosis and Regulating Oxidative Stress

Munakarmi

Chand

Shin

et al. 2020

IJMS

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3,3′-Diindolylmethane (DIM), a metabolic product of indole-3-carbinol extracted from cruciferous vegetables exhibits anti-inflammatory and anti-cancer properties. Earlier, the product has been demonstrated to possess anti-fibrotic properties; however, its protective effects on liver injury have not been clearly elucidated. In this study, we postulated the effects and molecular mechanisms of action of DIM on carbon tetrachloride (CCl4)-induced liver injury in mice. Acute liver injury was induced by a single intraperitoneal administration of CCl4 (1 ml/kg) into mice. DIM was injected via subcutaneous route for three days at various doses (2.5, 5 and 10 mg/kg) before CCl4 injection. Mice were sacrificed and serum was collected for quantification of serum transaminases. The liver was collected and weighed. Treatment with DIM significantly reduced serum transaminases levels (AST and ALT), tumor necrosis factor-α (TNF-α) and reactive oxygen species (ROS). CCl4- induced apoptosis was inhibited by DIM treatment by the reduction in the levels of cleaved caspase-3 and Bcl2 associated X protein (Bax). DIM treated mice significantly restored Cytochrome P450 2E1, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression in CCl4 treated mice. In addition, DIM downregulated overexpression of hepatic nuclear factor kappa B (NF-κB) and inhibited CCl4 mediated apoptosis. Our results suggest that the protective effects of DIM against CCl4- induced liver injury are due to the inhibition of ROS, reduction of pro-inflammatory mediators and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Indole-3-Carbinol Derivative DIM Mitigates Carbon Tetrachloride-Induced Acute Liver Injury in Mice by Inhibiting Inflammatory Response, Apoptosis and Regulating Oxidative Stress

Munakarmi

Chand

Shin

et al. 2020

IJMS

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“…CCl 4 can directly induce oxidative stress and triggers inflammatory cells by exposure to free radicals and toxic debris in mice [ 30 ]. Therefore, liver damage might be greatly propagated by releasing various inflammatory mediators from inflammatory cells after oxidative damage activation [ 36 ]. TNF-α and IL-1β are the most representative pro-inflammatory cytokines in inflammatory factors, and many studies have also shown that IL-1β and TNF-α play key roles in the development and maintenance of inflammation, while inflammatory cytokines are horizontally increased, which is related to liver disease [ 36 , 37 ].…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, liver damage might be greatly propagated by releasing various inflammatory mediators from inflammatory cells after oxidative damage activation [ 36 ]. TNF-α and IL-1β are the most representative pro-inflammatory cytokines in inflammatory factors, and many studies have also shown that IL-1β and TNF-α play key roles in the development and maintenance of inflammation, while inflammatory cytokines are horizontally increased, which is related to liver disease [ 36 , 37 ]. Inflammatory mediators such as TNF-α are up-regulated and might induce liver damage via multiple cytotoxic mechanisms [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

The Liver Protection Effects of Maltol, a Flavoring Agent, on Carbon Tetrachloride-Induced Acute Liver Injury in Mice via Inhibiting Apoptosis and Inflammatory Response

et al. 2018

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The purpose of this research was to evaluate whether maltol could protect from hepatic injury induced by carbon tetrachloride (CCl4) in vivo by inhibition of apoptosis and inflammatory responses. In this work, maltol was administered at a level of 100 mg/kg for 15 days prior to exposure to a single injection of CCl4 (0.25%, i.p.). The results clearly indicated that the intrapulmonary injection of CCl4 resulted in a sharp increase in serum aspartate transaminase (AST) and alanine transaminase (ALT) activities, tumor necrosis factor-α (TNF-α), irreducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-κB) and interleukin-1β (IL-1β) levels. Histopathological examination demonstrated severe hepatocyte necrosis and the destruction of architecture in liver lesions. Immunohistochemical staining and western blot analysis suggested an accumulation of iNOS, NF-κB, IL-1β and TNF-α expression. Maltol, when administered to mice for 15 days, can significantly improve these deleterious changes. In addition, TUNEL and Hoechst 33258 staining showed that a liver cell nucleus of a model group diffused uniform fluorescence following CCl4 injection. Maltol pretreatment groups did not show significant cell nuclear condensation and fragmentation, indicating that maltol inhibited CCl4-induced cell apoptosis. By evaluating the liver catalase (CAT), glutathione (GSH), superoxide dismutase (SOD) activity, and further using a single agent to evaluate the oxidative stress in CCl4-induced hepatotoxicity by immunofluorescence staining, maltol dramatically attenuated the reduction levels of hepatic CAT, GSH and SOD, and the over-expression levels of CYP2E1 and HO-1. In the mouse model of CCl4-induced liver injury, we have demonstrated that the inflammatory responses were inhibited, the serum levels of ALT and AST were reduced, cell apoptosis was suppressed, and liver injury caused by CCl4 was alleviated by maltol, demonstrating that maltol may be an efficient hepatoprotective agent.

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“…It has been found that TNF-α is one of the main cytokines in the occurrence and development of hepatic inflammatory injury. It can promote the production and release of many other cytokines and eventually form a cytokine network to expand the inflammatory chain reaction [31,32]. IL-6, produced by macrophages and monocytes, participates in the process of inflammatory damage and plays an important role in the local inflammatory response of the liver [33].…”

Section: Discussionmentioning

confidence: 99%

Hepatoprotective effects and mechanisms of Ixeris denticulate water extract on liver cirrhosis in experimental rat

Zhu

Liu

Chen

et al. 2020

BMC Complement Med Ther

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Background: To explore the protective effect and mechanisms of Ixeris denticulate water extract (IDWE) in the development of liver cirrhosis in experimental rat. Methods: Sixty rats were randomly divided into five groups: control group, model group and IDWE (2, 4 and 8 g/ kg) treatment groups. Alanine transferase (ALT), aspartate transaminase (AST), albumin (ALB), tumor necrosis factoralpha (TNF-α), Interleukin (IL)-6 and IL-8 in serum and superoxide dismutase (SOD), malondialdehyde (MDA) in liver tissue were evaluated, respectively. The liver index, liver morphology and liver histopathological analysis were detected as a supportive data. The liver protein expression of Bcl-2 and Bax were assessed by western blot, and NF-κB p65 protein expression was determined by immunohistochemistry analysis. Results: The result showed that a significantly decrease in the levels of serum AST, ALT and serum inflammatory factors TNF-α, IL-6 and IL-8 in IDWE-treated rats. The levels of serum ALB and SOD in liver tissue were markedly increased after IDWE treated, compared with model rats. Furthermore, IDWE-treated group also exhibited a downregulated protein expression of NF-κB p65 and Bax, up-regulated Bcl-2 protein expression. Conclusions: IDWE could effectively alleviate the course of liver cirrhosis in rat model, which may be a potent hepatoprotective agent in clinical therapy in the future.

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Diterpenoid trigonoreidon B isolated from Trigonostemon reidioides alleviates inflammation in models of LPS-stimulated murine macrophages and inflammatory liver injury in mice

Cited by 18 publications

References 40 publications

Indole-3-Carbinol Derivative DIM Mitigates Carbon Tetrachloride-Induced Acute Liver Injury in Mice by Inhibiting Inflammatory Response, Apoptosis and Regulating Oxidative Stress

Indole-3-Carbinol Derivative DIM Mitigates Carbon Tetrachloride-Induced Acute Liver Injury in Mice by Inhibiting Inflammatory Response, Apoptosis and Regulating Oxidative Stress

The Liver Protection Effects of Maltol, a Flavoring Agent, on Carbon Tetrachloride-Induced Acute Liver Injury in Mice via Inhibiting Apoptosis and Inflammatory Response

Hepatoprotective effects and mechanisms of Ixeris denticulate water extract on liver cirrhosis in experimental rat

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