• The Korea Journal of Herbology
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• v.21 no.3
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• pp.69-74
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• 2006

Objectives : This study was undertaken to determine if a combined(SPe) has a protective effect against functional failure induced by $CCl_4$ in rat liver. Methods : Acute liver injury which initiated from free radical induced by $CCl_4$, were applied to rats and data were obtained. Liver injury was estimated by measuring aspartate aminotransferase(AST) and alanine aminotransferase(ALT) activity in serum. Lipid peroxidation was examined by measuring malondialdehyde, a product of lipid peroxidation. GSH activities in liver tissues were also measured. Results : When rats were treated intraperitoneally with $CCl_4$, serum AST and ALT were increased compared with the control, which was significantly inhibited by pretreatment of SPe. SPe also prevented reduction in GSH induced by $CCl_4$. Conclusion : Above results suggest that SPe exerts protective effect against $CCl_4$ by its antioxidant action in liver tissues. Thus, SPe may be used in prevention and treatment of drug-induced liver cell injury. However, the precise mechanisms of SPe protection remain to be determined.

• Korean Journal of Veterinary Research
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• v.50 no.2
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• pp.145-149
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• 2010

This study was carried out to find whether phenidone (1-phenyl-3-pyrazolidinone), a cyclooxygenase as well as a lipoxygenase inhibitor, exhibits the preventive effect on carbon tetrachloride $(CCl_{4})-induced$ acute liver injury in rats. Rats were pretreated with phenidone at a dose of 50 or 200 mg/kg (p.o.) once daily for 3 consecutive days before $CCl_{4}$ administration. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Malondialdehyde (MDA) production was determined as an index of lipid peroxidation in the liver and serum. The histopathological changes in the liver were also examined in each group. The reduction in body weights was significantly inhibited in the phenidone-treated group than in the $CCl_{4}$ control group. Significant increase in the relative liver weights of the phenidone-treated groups was observed compared with either the vehicle or $CCl_{4}$ groups. Elevation of serum AST and ALT activities occurred after $CCl_{4}$ treatment was significantly attenuated by the pretreatment with phenidone. The elevation of MDA levels in liver and serum were completely inhibited in phenidone-treated groups. The protective effects on phenidone-treated groups were confirmed histopathologically. These results suggest that phenidone may be a useful protector through modulation of hepatic inflammation in $(CCl_{4})-induced$ acute liver injury.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.6
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• pp.659-670
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• 2017

Oxidative stress and inflammation are key factors responsible for progression of liver injury. A variety of functions of oyster hydrolysate (OH) are affected by their antioxidant and anti-inflammatory activities. However, little is known regarding the effects of OH on a liver injury model. This study was performed to evaluate the effects of OH on acute liver injury induced by lipopolysaccharide/D-galactosamine (LPS/D-GalN) in mice. Experimental groups were divided into six groups as follows (each group, n=10): control (saline), LPS/D-GalN, LPS/D-GalN+OH (100 mg/kg), LPS/D-GalN+OH (200 mg/kg), LPS/D-GalN+OH (400 mg/kg), and LPS/D-GalN+silymarin (25 mg/kg, positive control). The experimental acute liver injury model was induced with LPS ($1{\mu}g/kg$) and D-GalN (400 mg/kg). We first analyzed antioxidant and anti-inflammatory activities in OH. OH showed high DPPH and ABTS radical scavenging activities and reduced ROS generation in Chang cells in a dose-dependent manner. In addition, OH showed anti-inflammatory activities, such as inhibition of cyclooxygenase-2 and 5-lipooxygenase. Treatment with OH down-regulated tumor necrosis factor $(TNF)-{\alpha}$, interleukin (IL)-6, and $IL-1{\alpha}$ expression levels in LPS-stimulated RAW264.7 cells. OH significantly reduced LPS/D-GalN-induced increases in the concentrations of alanine transaminase and aspartate aminotransferase in serum. In the LPS/D-GalN group, liver tissues exhibited apoptosis of hepatocytes with hemorrhages. These pathological alterations were ameliorated by OH treatment. Consistently, hepatic catalase activity was low in the LPS/D-GalN group compared to the control group, and catalase activity was significantly restored by OH treatment (P<0.05). Furthermore, OH markedly reduced the LPS/D-GalN-induced increase in $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 levels in liver tissue. Taken together, these results show that OH has hepatoprotective effects on LPS/D-GalN-induced acute liver injury via inhibition of oxidative stress and inflammation, suggesting that OH could be used as a health functional food and potential therapeutic agent for acute liver injury.

• Journal of Nutrition and Health
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• v.54 no.2
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• pp.224-237
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• 2021

Purpose: Paeonia Radix Alba is a traditional herbal medicine used to treat the liver and the spleen. Many studies have reported that Paeonia Radix Alba extract (PR) affects liver injury, but there has been no study on liver injuries induced by thioacetamide (TAA). Therefore, we aimed at evaluating the effect of PR on a TAA-induced acute liver injury (ALI) model. Methods: The antioxidant activity of PR was assayed by the content of total polyphenol, total flavonoid, 1,1-diphenyl-2'-picrylhydrazyl (DPPH), and 2,2'-azino-bis (3-ethylbenzo-thiazoline-6-sulfonicacid) (ABTS) radical scavenging activities in vitro test. ALI was induced via-intraperitoneal injection of TAA (200 mg/kg body weight) for three consecutive days. Also, silymarin (100 mg/kg body weight) and PR (100 or 200 mg/kg body weight) were administered at 1 hours 30 minutes prior to TAA treatment. The levels of ammonia, glutamic oxaloacetic transaminase (GOT), and glutamic pyruvic transaminase (GPT) were analyzed using an assay kit. The expressions of antioxidant proteins including Nrf2, Keap1, HO-1, SOD, catalase, and GPx-1/2 and oxidative stress-related proteins including NOX2, p47^phox, and p22^phox were evaluated by the western blot analysis. Results: PR showed excellent antioxidant activity in vitro. TAA administration increased the levels of ammonia, GOT, and GPT in the ALI control group compared to the normal group, whereas it was significantly reduced by PR pretreatment. Moreover, NADPH oxidase protein expressions were upregulated after TAA treatment, while the elevated expressions were inhibited by PR pretreatment. The expressions of antioxidant protein were downregulated in the ALI control group, whereas Nrf2 activation in the PR group was accompanied by increased levels of antioxidant enzymes. Conclusion: PR administration increased the antioxidant enzymes via activation of the Keap1/Nrf2 pathway and inhibited the protein levels of NADPH oxidase factors. Taken together, these results showed that PR treatment may be considered to ameliorate acute liver injury induced by TAA.

• Biomolecules & Therapeutics
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• v.32 no.3
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• pp.341-348
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• 2024

Endoplasmic reticulum (ER) stress plays a crucial role in liver diseases, affecting various types of hepatic cells. While studies have focused on the link between ER stress and hepatocytes as well as hepatic stellate cells (HSCs), the precise involvement of hepatic macrophages in ER stress-induced liver injury remains poorly understood. Here, we examined the effects of ER stress on hepatic macrophages and their role in liver injury. Acute ER stress led to the accumulation and activation of hepatic macrophages, which preceded hepatocyte apoptosis. Notably, macrophage depletion mitigated liver injury induced by ER stress, underscoring their detrimental role. Mechanistic studies revealed that ER stress stimulates macrophages predominantly via the PERK signaling pathway, regardless of its canonical substrate ATF4. hnRNPA1 has been identified as a crucial mediator of PERK-driven macrophage activation, as the overexpression of hnRNPA1 effectively reduced ER stress and suppressed pro-inflammatory activation. We observed that hnRNPA1 interacts with mRNAs that encode UPR-related proteins, indicating its role in the regulation of ER stress response in macrophages. These findings illuminate the cell type-specific responses to ER stress and the significance of hepatic macrophages in ER stress-induced liver injury. Collectively, the PERK-hnRNPA1 axis has been discovered as a molecular mechanism for macrophage activation, presenting prospective therapeutic targets for inflammatory hepatic diseases such as acute liver injury.

• The Journal of Korean Medicine
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• v.44 no.4
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• pp.163-169
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• 2023

Methods: This study presents a comprehensive case study of an elderly male diagnosed with acute kidney injury (AKI) resulting from severe dehydration, supported by an extended follow-up with laboratory findings. Results: An 83-year-old male patient experienced severe diarrhea overnight, leading to hospitalization due to symptoms of dehydration and hypotension. His laboratory results displayed a typical AKI pattern, including a significant increase in creatinine levels (5.19 mg/dL) and the presence of hyperkalemia and hyponatremia. Following general treatments, including the administration of an herbal drug (Bulhwangeumjeonggi-san), the estimated glomerular filtration rate (eGFR) improved from 10 ml/min (Stage 5) to 34 ml/min (Stage 3) within five days when he was discharged. Although subsequent eGFR tests, conducted one and two months later as an outpatient, revealed an improvement of 42 ml/min, the patient still experienced mild chronic dysfunction as a consequence. Conclusion: This study presents a noteworthy case of acute kidney injury attributed to severe dehydration, emphasizing the importance of medical awareness regarding diarrhea-induced kidney function impairment, especially in the elderly population.

• The Korea Journal of Herbology
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• v.36 no.2
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• pp.31-42
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• 2021

Objectives : This study was undertaken to investigate the hepatoprotective effect of Spatholobi Caulis water extract (SC) to thioacetamide (TAA)-induced acute liver injury (ALI) in rats. Methods : The rats were injected intraperitoneally with TAA (200 mg/kg body weight) and orally administered SC (100 or 200 mg/kg b.w.) daily for 3 days. Liver biomarkers were assessed by serum glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and ammonia levels. Malondialdehyde (MDA) was measured both serum and liver tissue. In addition, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, anti-oxidant, and inflammation-related proteins were investigated by western blot analysis. Histological examination further confirmed though hematoxylin and eosin stain. Results : The SC treatment reduced liver function markers like GOT and GPT and also remarkably decreased ammonia level. Moreover, the elevated MDA level in TAA-induced group was significantly reduced by SC treatment. NADPH oxidase expression associated with oxidative stress including NOX2, NOX4, and p47phox markedly inhibited by SC administration. SC treatment exerted anti-oxidant effect through the increase of anti-oxidant enzyme including superoxide dismutase (SOD), Catalase, and heme oxygenase-1 (HO-1). The protein expressions of inflammatory cytokines such as tumor necrosis factor-�� (TNF-��), IL-6, and IL-1�� induced by nuclear factor-kappa B (NF-��B) activation were modulated through blocking the phosphorylation of inhibitor of nuclear factor ��B�� (I��B)��. SC treatment also improved histological alterations. Conclusion : These findings suggested that SC administration may be a potential candidate for the prevention or treatment of ALI.

• Journal of Trauma and Injury
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• v.28 no.1
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• pp.34-38
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• 2015

The case of a patient with a transfusion-related acute lung injury (TRALI) to whom extracorporeal membrane oxygenation (ECMO) had been applied is reported. A 55-year-old male injured with liver laceration (grade 3) without chest injury after car accident. He received lots of blood transfusion and underwent damage control abdominal surgery. In the immediate postoperative period, he suffered from severe hypoxia and respiratory acidosis despite of vigorous management such as 100% oxygen with mechanical ventilation, high PEEP and muscle relaxant. Finally, ECMO was applied to the patients as a last resort. Aggressive treatment with ECMO improved the oxygenation and reduced the acidosis. Unfortunately, the patient died of liver failure and infection. TRALI is a part of acute respiratory distress syndrome (ARDS). The use of ECMO for TRALI induced severe hypoxemia might be a useful option for providing time to allow the injured lung to recover.

• The Journal of Internal Korean Medicine
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• v.32 no.3
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• pp.444-450
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• 2011

Recently, acute toxic liver injury has been reported to be the most common cause of acute hepatitis. We witnessed one case of hepatic injury which suggested drug-induced hepatitis by herbal medication (Gamiyukgunja-tang). This patient, diagnosed cerebral infarction, was treated with herbal medication and physical therapy for improvement of right hemiparesis. In the course of treatment, this patient showed elevation of serum transaminase (ALT 129 IU/L, AST 150 IU/L), alkaline phosphatase (ALP 261 IU/L), and total bilirubin (2.0 IU/L), so we supposed toxic hepatitis by herbal medication. Saenggangeonbi-tang was administered for 8 days, ALT, AST, ALP, total bilirubin decreased within normal limits.

• Korean Journal of Acupuncture
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• v.20 no.4
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• pp.41-52
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• 2003

Objectives : Circii Herba has been used as a natural drug for the treatment of stress digestive system disease. The aim of this study is to investigate the role of Circii Herba aqua-acupuncture solution (CHAS) in experimental oxidative liver injury. Methods : In order to investigate the effects of CHAS on acute liver injury, male ICR mice were pretreated with CHAS(0.2 ml/mouse/day) at the loci of BL18 and CV12 for 6days, starved for 24hrs, and administerated acetaminophen(500 mg/kg, i.p.). After acetaminophen administeration, mice were sacrificed, and the liver was removed, rinsed with ice-cold $1.15{\%}$ KCI buffer, and homogenized at $4^{\circ}C$. Fractions(fraction Ⅰ, Ⅱ, Ⅲ) were isolated by differential centrifugation. Lipidperoxide, total SH, and glutathione(GSH) levels were measured in the Fraction Ⅰ. In addition, activities of hepatic enzyme, such as catalase, glutathione peroxidase(GSH-Px) were measured in the Fraction Ⅱ, and glutathione S-transferase(GST) was measured in the Fraction Ⅲ. Results : In vivo treatment of CHAS(BL18 and CV12) showed effective inhibition of acetaminophen induced lipid peroxidation, and showed elevations of total SH, GSH level, catalase, GSH-Px, GST activities. Conclusions : These results suggested that CHAS might suppress the formation of oxidative metabolites, and prevent acetaminophen induced hepatotoxicity.