Protective effects of active hexose correlated compound in a rat model of liver injury after hepatectomy

Nakatake, Richi; Tanaka, Yoshito; Ueyama, Yosuke; Miki, Hirokazu; Ishizaki, Morihiko; Matsui, Kosuke; Kaibori, Masaki; Okumura, Tadayoshi; Nishizawa, Mikio; Kon, Masanori

doi:10.31989/ffhd.v6i11.305

Cited by 10 publications

(15 citation statements)

References 28 publications

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“…Administration of an effective functional food or Kampo medicine improves the survival of endotoxemia model animals. For example, a standardized extract of cultured Lentinula edodes mycelia (AHCC®︎) had protective effects on endotoxemia model rats with liver failure after hepatectomy [12]. The mRNAs encoding pro-inflammatory mediators in the partial hepatectomy/LPS model rats expressed more than those in the Dgalactosamine/LPS model rats [48].…”

Section: Evaluation and Discussion Of Anti-inflammatory Effects Using Animal Modelsmentioning

confidence: 99%

Assessment of anti-inflammatory effects of Japanese Kampo medicine versus functional foods

Nishizawa¹,

Okumura²,

Ikeya³

2019

FFHD

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Background: Traditional Japanese drugs called Kampo medicine are widely used in Japan. Each Kampo medicine consists of several crude drugs, most of which are derived from medicinal plants. Clinical administration has empirically evaluated the effects of Kampo medicine In contrast, functional foods are prepared from foods and edible plants (e.g., herbs, vegetables, and fruits). Due to the relatively low content of a pharmacologically active constituents in functional foods, their effectiveness has not been well evaluated and thus should be better investigated. Kampo medicine and functional foods have beneficial effects for humans, and many of them exhibit anti-inflammatory effects. Here, we discuss the principles and methods to assess the anti-inflammatory effects of functional foods and Kampo medicine.To investigate pharmacological effects of functional foods and Kampo medicines, their constituents should be isolated to identify their chemical structures. Cell-based studies are commonly performed to evaluate anti-inflammatory effects of the constituents in Kampo medicine and functional foods. Primary cultured rat hepatocytes are used and produce pro-inflammatory mediators, including nitric oxide. When an extract from a Kampo medicine, functional food, or a respective constituent is added to the medium, pro-inflammatory mediator production decreases, and the anti-inflammatory activity is estimated. Animal experiments have been performed using disease models, such as the endotoxemia model for animals, to which bacterial endotoxin is administered. Administering an effective functional food or Kampo medicine improves the survival of the model animals. The action of the anti-inflammatory effects of functional foods and Kampo medicines can be investigated by the above-mentioned methods. The studies using cells and animals will provide a basis for the safe and effective use of functional foods and Kampo medicine in humans to treat diseases or improve health conditions.Keywords: herbal drug, Kampo medicine, nitric oxide, inflammation, hepatocytes.

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Section: Evaluation and Discussion Of Anti-inflammatory Effects Using Animal Modelsmentioning

confidence: 99%

Assessment of anti-inflammatory effects of Japanese Kampo medicine versus functional foods

Nishizawa¹,

Okumura²,

Ikeya³

2019

FFHD

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Section: Discussionmentioning

confidence: 93%

“…In animal liver injury models caused by various insults, such as ischemia-reperfusion, partial hepatectomy, and endotoxin shock, we found that drugs [15][16][17][18][19] and functional foods [20] demonstrated liver-protective effects. These drugs and functional foods led to higher survival rates and a reduction in various cytokine production, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and cytokine-induced neutrophil chemoattractant (CINC)-1 (human IL-8 analogue) [15][16][17][18][19]. These clinical drugs [17,21,22,23] and others, such as L-glutamic acid (component of GSH) [24], curcumin [25], and active hexose correlated compound [26], inhibited induction of iNOS and NO production in primary cultures of rat hepatocytes stimulated by IL-1β ("in vitro liver injury model").…”

Section: Discussionmentioning

confidence: 93%

Glutathione inhibits expression of the proinflammatory biomarker inducible nitric oxide synthase in hepatocytes

Nakatake¹,

Kotsuka²,

Hashimoto³

et al. 2018

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Background: Intracellular glutathione (GSH) plays an important regulatory role in the host response to liver injury. However, there have been few scientific reports on the anti-inflammatory effects of GSH. In the inflamed liver, proinflammatory cytokines stimulate liver cells, followed by expression of inducible nitric oxide synthase (iNOS). Excessive nitric oxide (NO) levels produced by iNOS are one of the factors involved in liver injury. Therefore, inhibiting iNOS induction is important for preventing liver injury. This study aimed to investigate the protective effects of GSH on the liver by examining interleukin (IL)-1β-stimulated hepatocytes.Methods: Primary cultured rat hepatocytes were treated with IL-1β in the presence or absence of GSH. Induction of iNOS and its signaling pathway were analyzed.Results: Addition of GSH decreased IL-1β-induced iNOS protein and mRNA expression levels, which resulted in inhibition of NO production. GSH also decreased tumor necrosis factor (TNF)-α and IL-6 mRNA expression. GSH blocked “type I IL-1 receptor upregulation”, one of the essential signaling pathways for iNOS induction, through inactivation of an upstream kinase, phosphatidylinositol 3-kinase/Akt. In contrast, GSH had no effects on degradation of IκB and activation of NF-ĸB (nuclear translocation and its DNA binding). Transfection experiments revealed that GSH reduced iNOS mRNA levels at the promoter transactivation and mRNA stabilization steps. Delayed administration of GSH after IL-1β addition also inhibited iNOS induction. Conclusions: Our study suggests that GSH affects induction of inflammatory mediators, including iNOS and TNF-α, indicating its therapeutic potential for organ injuries, especially for the liver.Keywords: glutathione, inducible nitric oxide synthase, liver injury, primary cultured hepatocytes, type I interleukin-1 receptor, tumor necrosis factor-α

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“…There are several experimental animal models of endotoxemia and sepsis with liver failure, including two that we reported previously: simultaneous administration of D-galactosamine and LPS (GaIN/LPS) [3][4][5] and a partial (70%) hepatectomy followed by LPS administration (PH/LPS) 6, 7 . In our previous studies, high doses of LPS, such as ≥50 µg/kg and ≥250 µg/kg, resulted in poor survival (less than 10%) in two models of GalN/LPS and PH/LPS, respectively.…”

Section: Introductionmentioning

confidence: 99%

“…In both sepsis models, nitric oxide (NO)/inducible nitric oxide synthase (iNOS) and in ammatory mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and cytokine-induced neutrophil chemoattractant 1/chemokine (C-X-C motif) ligand 1 (CINC-1/CXCL-1) (IL-8 rat analogue) are excessively induced in hepatocytes within 3 h of LPS injection [3][4][5][6][7] . Excessive NO production by iNOS contributes to liver injury 8,9 .…”

Section: Introductionmentioning

confidence: 99%

Omeprazole increases survival via different mechanisms in two rat models of liver injury

Kotsuka

Hashimoto

Nakatake

et al. 2021

Preprint

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Omeprazole (OMZ) is a proton pump inhibitor (PPI) that is used to reduce gastric acid secretion, but little is known about its possible liver protective effects. This study investigated whether OMZ has beneficial effects in rat septic models of lipopolysaccharide (LPS)-induced liver injury after D-galactosamine (GalN) treatment and 70% hepatectomy (PH), and to determine the mechanisms of OMZ in an in vitro model of liver injury. In the in vivo models, the effects of OMZ were examined 1 h before treatment. OMZ increased survival and decreased tumor necrosis factor-alpha, inducible nitric oxide synthase, cytokine-induced neutrophil chemoattractant 1, interleukin (IL)-6, and IL-1β mRNA expression, and increased IL-10 mRNA expression in the livers of both GaIN/LPS- and PH/LPS-treated rats. Necrosis and apoptosis were inhibited by OMZ in GaIN/LPS rats, but OMZ had no effects on necrosis in PH/LPS rats. Primary rat hepatocytes were treated with IL1-β in the presence or absence of OMZ (in vitro model). OMZ inhibited iNOS induction partially through suppression of NF-κB signaling in hepatocytes. Furthermore, OMZ inhibited the induction of several inflammatory mediators, resulting in the prevention of LPS-induced liver injury after GalN liver failure and PH, although OMZ showed different doses and mechanisms in the two models.

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Protective effects of active hexose correlated compound in a rat model of liver injury after hepatectomy

Cited by 10 publications

References 28 publications

Assessment of anti-inflammatory effects of Japanese Kampo medicine versus functional foods

Assessment of anti-inflammatory effects of Japanese Kampo medicine versus functional foods

Glutathione inhibits expression of the proinflammatory biomarker inducible nitric oxide synthase in hepatocytes

Omeprazole increases survival via different mechanisms in two rat models of liver injury

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