• 농업과학연구
• /
• 제51권2호
• /
• pp.147-158
• /
• 2024

Hepatic fibrosis refers to the scarring of liver tissue, often resulting from chronic liver injury or inflammation. It is characterized by excessive deposition of extracellular matrix proteins, impairing liver function and potentially progressing to cirrhosis if left untreated. To improve the liver functions, Cordyceps militaris, a species of parasitic fungus known for its medicinal properties, is used in the form of extract. It has been traditionally used in Chinese medicine to boost energy, improve stamina, and support overall health. In this study, we investigated the hepatoprotective effects of Cordyceps militaris extract powder in a liver injury model induced by hepatic fibrosis. Sprague-Dawley (SD) rats were administered Dimethylnitrosamine (DMN) to induce liver injury, and the hepatoprotective effects of Cordyceps militaris extract powder intake were assessed by comparing changes in liver enzyme levels and histological observations. Rats injected with DMN were orally administered Cordyceps militaris extract powder at doses of 0, 125, 250, and 500 mg·kg^-1·day^-1 for three weeks. After three weeks of treatment, no significant differences were observed in hematological, clinical chemical, organ weight, gross examination, or microscopic examination between the DMN-alone group and the Cordyceps militaris extract powder-treated group. In conclusion, hepatoprotective effects against DMN-induced liver injury in SD rats treated with Cordyceps militaris extract powder were not observed under this study condition.

• Journal of Ginseng Research
• /
• 제43권2호
• /
• pp.196-208
• /
• 2019

Background: Nonalcoholic steatohepatitis (NASH) is one of the chronic inflammatory liver diseases and a leading cause of advanced liver fibrosis, cirrhosis, and hepatocellular carcinoma. The main purpose of this study was to clarify the effects of GBCK25 fermented by Saccharomyces servazzii GB-07 and pectinase, on NASH severity in mice. Methods: Six-wk-old male mice were fed either a normal diet (ND) or a Western diet (WD) for 12 wks to induce NASH. Each group was orally administered with vehicle or GBCK25 once daily at a dose of 10 mg/kg, 20 mg/kg, 100 mg/kg, 200 mg/kg, or 400 mg/kg during that time. The effects of GBCK25 on cellular damage and inflammation were determined by in vitro experiments. Results: Histopathologic analysis and hepatic/serum biochemical levels revealed that WD-fed mice showed severe steatosis and liver injury compared to ND-fed mice. Such lesions were significantly decreased in the livers of WD-fed mice with GBCK25 administration. Consistently, mRNA expression levels of NASH-related inflammatory-, fibrogenic-, and lipid metabolism-related genes were decreased in the livers of WD-fed mice administered with GBCK25 compared to WD-fed mice. Western blot analysis revealed decreased protein levels of cytochrome P450 2E1 (CYP2E1) with concomitantly reduced activation of c-Jun N-terminal kinase (JNK) in the livers of WD-fed mice administered with GBCK25. Also, decreased cellular damage and inflammation were observed in alpha mouse liver 12 (AML12) cells and RAW264.7 cells, respectively. Conclusion: Administration of GBCK25 ameliorates NASH severity through the modulation of CYP2E1 and its associated JNK-mediated cellular damage. GBCK25 could be a potentially effective prophylactic strategy to prevent metabolic diseases including NASH.

• 한국한의학연구원논문집
• /
• 제11권2호
• /
• pp.97-111
• /
• 2005

This study was performed to evaluate anti-thrombotic activities and anti-inflammatory effects of ChungyeolHaedogHwaeoTang water extract(CHHT). The results were summarized as follows. In experiment of anti-thrombotic effect; 1. CHHT inhibited human platelet aggregation induced by ADP and epinephrine as compared with the control group, and inhibited pulmonary embolism induced by collagen and epinephrine (inhibitory rate is 37.5%). 2. CHHT increased platelet number significantly, and also CHHT shortened PT and APTT significantly as compared with the control group in thrombus model induced by dextran. In experiment of anti-inflammatory effect; 3. CHHT inhibited $IL-1{\beta}$, IL-6, TNF-${\alpha}$, COX-2 and NOS-II mRNA expression as compared with the control group in a concentration-dependent degree, and inhibited NO production significantly at 50, 100 ${\mu}g/ml$, and also inhibited ROS production in a concentration-dependent degree as compared with the control of group in RAW 264.7 cell line. 4. CHHT inhibited $IL-1{\beta}$, IL-6 and TNF-${\alpha}$ production significantly in serum of acute inflammation-induced mice, and decreased $IL-1{\beta}$, IL-6 and TNF-${\alpha}$ production in spleen tissue, and also decreased $IL-1{\beta}$, and IL-6 production in liver tissue, but increased TNF-${\alpha}$ production in liver tissue of acute inflammation-induced Balb/c mice. 5. CHHT increased survival rate from the 3rd day in ICR mice with lethal endotoxemia induced by LPS. These results suggest that CHHT can be useful in treating diverse female diseases caused by thrombosis and inflammation such as menstrual pain, menstrual disorder, leukorrhea, vaginitis, cervicitis, pelvic inflammatory disease and so on.

• 대한한방내과학회지
• /
• 제24권1호
• /
• pp.113-122
• /
• 2003

Objective : The aim of this study was to evaluate the efficacy of Gagamchunggan-tang on anti-inflammation reaction with lipopolysaccharide (LPS)-induced HepG2 cell. Method : We examined the effects of the Gagamchunggan-tang, a traditional drug for liver inflammation, on the process of lipopolysaccharide(LPS)-induced nuclear factor-${\kappa}Bp65(NF-{\kappa}Bp65)$ activation in HepG2 cell. SDS-PAGE, Western blotting, Immunofluorescence staining were studied. Results : Immunoblot analysis showed that the level of nucleic $NF-{\kappa}Bp65$ was rapidly up-regulated and cytosolic inhibitory $I-{\kappa}B{\alpha}$ was down-regulated by LPS challenge. While Gagamchunggan-tang inhibited an increase of $NF-{\kappa}Bp65$ and degradation of $I-{\kappa}B{\alpha}$ in HepG2 cell. Besides LPS-induced expression of a group of genes, such as tumor necrosis factor-${\alpha}(TNF-{\alpha})$, inducible nitric oxide synthase(iNOS) and cyclooxygenase-2 (COX-2), are repressed by Gagamchunggan-tang. It may be concluded that Gagamchunggan-tang attenuates the progress of LPS-induced inflammation by reduction of $NF-{\kappa}Bp65$ activation. Conclusion : The Gagamchunggan-tang would be useful as a therapeutic agent for endotoxin-induced liver disease.

• 동의생리병리학회지
• /
• 제20권4호
• /
• pp.957-965
• /
• 2006

This study was peformed to evaluate antithrombotic activities and anti-inflammatory effects of Kami-BoyangHwanoh-Tang(KBHT). The major findings were summarized as follows. In experiment of anti-thrombotic effect; KBHT inhibited human platelet aggregation induced by ADP and epinephrine as compared with the control group and inhibited pulmonary embolism induced by collagen and epinephrine (inhibitory rate is 50 %). KBHT increased platelet number significantly and also KBHT shortened PT and APTT significantly as compared with the control group in thrombus model induced by dextran. In experiment of anti-inflammatory effect; KBHT inhibited $IL-1{\beta}$, IL-6, $TNF-{\alpha}$, COX-2 and NOS-II mRNA expression as compared with the control group in a concentration-dependent degree, and inhibited NO production significantly at 50, $100\;{\mu}g/^{ml}$, and also inhibited ROS production in a concentration-dependent degree as compared with the control group in RAW 264.7 cell line. KBHT inhibited $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ production significantly in serum of acute inflammation-induced mice, and decreased $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ production in spleen tissue, and also decreased IL-6 and $TNF-{\alpha}$ production in liver tissue, but increased $IL-1{\beta}$ production in liver tissue of acute inflammation-induced mice. KBHT increased survival rate at 3rd day in mice with lethal endotoxemia induced by LPS. These results suggest that KBHT can be useful in treating diverse female diseases caused by thrombosis and inflammation such as endometrosis, myoma, pelvic congestion, chronic cervicitis, chronic pelvic inflammatory disease and so on.

• Biomolecules & Therapeutics
• /
• 제29권5호
• /
• pp.455-464
• /
• 2021

Uncontrolled inflammation is considered the pathophysiological basis of many prevalent metabolic disorders, such as nonalcoholic fatty liver disease, diabetes, obesity, and neurodegenerative diseases. The inflammatory response is a self-limiting process that produces a superfamily of chemical mediators, called specialized proresolving mediators (SPMs). SPMs include the ω-3-derived family of molecules, such as resolvins, protectins, and maresins, as well as arachidonic acid-derived (ω-6) lipoxins that stimulate and promote resolution of inflammation, clearance of microbes, and alleviation of pain and promote tissue regeneration via novel mechanisms. SPMs function by binding and activating G protein-coupled receptors, such as FPR2/ALX, GPR32, and ERV1, and nuclear orphan receptors, such as RORα. Recently, several studies reported that SPMs have the potential to attenuate lipid metabolism disorders. However, the understanding of pharmacological aspects of SPMs, including tissue-specific biosynthesis, and specific SPM receptors and signaling pathways, is currently limited. Here, we summarize recent advances in the role of SPMs in resolution of inflammatory diseases with metabolic disorders, such as nonalcoholic fatty liver disease and obesity, obtained from preclinical animal studies. In addition, the known SPM receptors and their intracellular signaling are reviewed as targets of resolution of inflammation, and the currently available information on the therapeutic effects of major SPMs for metabolic disorders is summarized.

• Asian Pacific Journal of Cancer Prevention
• /
• 제14권1호
• /
• pp.261-265
• /
• 2013

Scutellaria barbata D. Don (S. barbata), a traditional Chinese medicine, is used to treat cancers, inflammation, and urinary diseases. This study aimed to determine any protective effects of S. barbata crude extract (CE-SB) against rat liver tumorigenesis induced by diethylnitrosamine (DENA). Liver malfunction indices in serum were measured by biochemical examination. Hematoxylin and eosin staining was performed to examine liver pathology. Contents of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured in liver homogenates to evaluate oxidative stress. The levels of liver malfunction indices in the CE-SB groups, especially in the CE-SB high dose group, were lower than that of the model group (P<0.05). The results from histological examination indicated that the number of liver nodules in the CE-SB groups decreased compared with the model group (P<0.05). Content of MDA determined in liver was significantly decreased, and level of SOD elevated by CE-SB. CE-SB can inhibit experimental liver tumorigenesis and relieve hepatic injury in rats.

• 대한한방내과학회지
• /
• 제43권4호
• /
• pp.643-655
• /
• 2022

Objective: To investigate the protective effects of Haeganjeon on a thioacetamide (TAA)-induced liver fibrosis mouse model and to determine the Haegan-jeon signaling pathway. Methods: Mice were randomly divided into 4 groups: Normal group (Nor), TAA-induced liver fibrosis group (Con), TAA-induced liver fibrosis group administered 50 mg/kg silymarin (S50), TAA-induced liver fibrosis group administered 200 mg/kg Haegan-jeon (H200). The liver fibrosis mouse model was established by intraperitoneal injection with TAA three times a week for 8 weeks. During the 8 weeks, mice were orally administered silymarin and Haegan-jeon every day. At the end of the study, serum was collected to measure the levels of AST, ALT, ammonia, and myeloperoxidase (MPO). Liver tissue was harvested and analyzed by western blotting and Masson's trichrome staining. Results: Administration of Haegan-jeon suppressed the increase in serum levels of AST, ALT, ammonia, and MPO due to TAA-induced liver fibrosis. Compared to the Con group, the H200 group showed increases in antioxidant-related factors (Nrf2, HO-1, catalase, and GPx-1/2) and decreases in inflammatory-related factors (NF-κB p65, p-IκB-α, Cox-2, iNOS, TNF-α, and IL-1β) in western blots. The H200 treatment inhibited the expression of α-SMA and Collagen I. Conclusions: Haegan-jeon showed a hepatoprotective effect induced by activation of antioxidant-related factors, such as Nrf2, and it regulated the inflammation response by suppression of NF-κB.

• Biomolecules & Therapeutics
• /
• 제18권1호
• /
• pp.83-91
• /
• 2010

Bear bile has been used as a therapeutic for cerebral and coronary thrombosis, convulsion, hepatitis, jaundice, and abscess in traditional oriental medicine. In recent decades, the effects of bile acids on cancer, cholestasis, and liver injury have been investigated in many studies. In this study, we investigated the anti-inflammatory effects of whole bear bile (WBB) and its two major components, chenodeoxycholic acid (CDCA) and ursodeoxycholic acid (UDCA), on rectal inflammation in rats. Bile acids in WBB were quantitatively analyzed by HPLC. Rectal inflammation was induced in male Sprague-Dawley rats by insertion of croton oil-saturated cotton tips. WBB, UDCA or CDCA solution was orally administered to rats one hour after induction of rectal inflammation. Rats were sacrificed 4 or 24 hours after induction of rectal inflammation. The evaluation included measurement of weight and thickness of rectum and histopathologic examination of rectal tissue. Furthermore, we examined the inhibitory effect of WBB, UDCA or CDCA against NO production in LPS-stimulated RAW 264.7 cells. The contents of UDCA and CDCA in WBB were $39.26{\mu}g/mg$ and $47.11{\mu}g/mg$, respectively. WBB treatment significantly reduced the weight and thickness of rectum compared with UDCA or CDCA treatment. The inhibition of NO production by WBB, UDCA and CDCA in LPS-stimulated RAW 264.7 cells was much higher than that by the control. And, WBB treatment suppressed the induction of NO synthase in rectum homogenates. These results suggest that the anti-inflammatory effect of WBB is related to the suppression of NO synthase induction and the inhibition of NO production by UDCA, CDCA and other bile acids of WBB.

• Biomolecules & Therapeutics
• /
• 제28권4호
• /
• pp.344-353
• /
• 2020

This study aims to develop new potential therapeutic moracin M prodrugs acting on lung inflammatory disorders. Potential moracin M prodrugs (KW01-KW07) were chemically synthesized to obtain potent orally active derivatives, and their pharmacological activities against lung inflammation were, for the first time, examined in vivo using lipopolysaccharide (LPS)-induced acute lung injury model. In addition, the metabolism of KW02 was also investigated using microsomal stability test and pharmacokinetic study in rats. When orally administered, some of these compounds (30 mg/kg) showed higher inhibitory action against LPS-induced lung inflammation in mice compared to moracin M. Of them, 2-(3,5-bis((dimethylcarbamoyl)oxy)phenyl)benzofuran-6-yl acetate (KW02) showed potent and dose-dependent inhibitory effect on the same animal model of lung inflammation at 1, 3, and 10 mg/kg. This compound at 10 mg/kg also significantly reduced IL-1β concentration in the bronchoalveolar lavage fluid of the inflamed-lungs. KW02 was rapidly metabolized to 5-(6-hydroxybenzofuran-2-yl)-1,3-phenylene bis(dimethylcarbamate) (KW06) and moracin M when it was incubated with rat serum and liver microsome as expected. When KW02 was administered to rats via intravenous or oral route, KW06 was detected in the serum as a metabolite. Thus, it is concluded that KW02 has potent inhibitory action against LPS-induced lung inflammation. It could behave as a potential prodrug of moracin M to effectively treat lung inflammatory disorders.