Kim, Jin Hoo;Yang, Won Kyung;Lee, Su Won;Lyu, Yee Ran;Kim, Seung Hyung;Park, Yang Chun
The Journal of Internal Korean Medicine
/
v.41
no.3
/
pp.339-349
/
2020
Objective: This study aimed to evaluate anti-inflammatory and antitussive expectoration effects of Friltillariae Thunbergii Bulbus (FTB) in a mouse model. Materials and Methods: To evaluate the anti-inflammatory effects of the FTB, we conducted in vitro experiments using RAW264.7 cells. An MTT assay and enzyme-linked immunosorbent assay (ELISA) were carried out to examine the anti-inflammatory effects of FTB. The expectorant effect on phenol red secretion, the antitussive effect on cough induced by ammonia solution, and leukocyte increased inhibition effects in acute airway inflammation in the animal model were confirmed. Results: FTB did not show cytotoxicity in the experimental group at 10, 30, 50, 100, 300, or 500 ㎍/ml and significantly inhibited the increase of NO, TNF-α and IL-6 in the experimental groups at 30, 50, 100, 300, and 500 ㎍/ml concentrations. In sputum, cough, and acute airway inflammation animal models, FTB significantly increased phenol red secretion in the 400 mg/kg administration group. FTB significantly reduced the number of coughs and significantly increased cough delay time in both 200 and 400 mg/kg dose groups. FTB decreased the white blood cell count in BALF (bronchoalveolar lavage fluid) in the 400 mg/kg administration group. Conclusion: Our study revealed that FTB elicits antitussive and expectorant effects by inhibiting inflammatory cytokines, increasing sputum secretion, suppressing cough, and reducing inflammatory cells. We concluded that FTB is a highly promising agent for respiratory tract infection with therapeutic opportunities.
Journal of Physiology & Pathology in Korean Medicine
/
v.21
no.3
/
pp.671-678
/
2007
Diabetes is a disease in which the body does not produce or properly use insulin. Etiological studies of diabetes and its complications showed that oxidative stress might play a major role. Therefore, many efforts have been tried to regulate free oxygen radicals for treating diabetes and its complications. Gamigukihwandong-hwan has been known to be effective for the treatment of diabetes. The present study was carried out to investigate the effect of Gamigukihwandong-hwan on renal function, peroxynitrite (ONOO$^-$) scavenging activity and polyol pathway in streptozotocin-induced diabetic rats. The crushed Gamigukihwandong-hwan was extracted 3 times, each time with 3 volumes of methyl alcohol at 60$^{\circ}C$ for 24 h. The extract was filtered and evaporated under a reduced pressure using a rotary evaporator to yield 74.95 g. Gamigukihwandong-hwan extract was oral-administered 100 mg per 1 kg of body weight for 20 days to the diabetic rats induced by streptozotocin (60 mg/kg). The effects of Gamigukihwandong-hwan extract on the streptozotocin-induced diabetic rats were observed by measuring the serum level of glucose, insulin, lipid components, creatinine and BUN, and also the kidney levels of superoxide anion radical (${\cdot}O_2^-$), nitric oxide (NO) and ONOO$^-$, and also the enzyme activities involved in polyol pathway. The Effects of Gamigukihwandong-hwan on the streptozotocin-induced diabetic rats with regards to body weight, blood glucose and insulin levels, creatinine and BUN levels, total cholesterol and triglyceride levels, and HDL-cholesterol levels were all shown to be good enough to cure and prevent the diabetes and its complications. Gamigukihwandong-hwan inhibited the generation of ${\cdot}O_2^-$, NO and ONOO$^-$ in the kidney of streptozotocin-induced diabetic rats. Renal aldose reductase and sorbitol dehydrogenase activities were increased in the streptozotocin-induced diabetic rats, whereas the ones in the Gamigukihwandong-hwan administered group among the streptozotocin-induced diabetic rats were reversed toward the natural activities. Gamigukihwandong-hwan might inhibit the development of diabetic nephropathy by scavenging reactive oxygen and nitrogen species, thereby by reducing oxidative stresses and also by regulating the activities of polyol pathway enzymes, all of which could help to recover the function of kidney.
Kim, Wang-In;Youn, Dae-Hwan;Choi, Chan-Hun;Na, Chang-Su
Korean Journal of Acupuncture
/
v.29
no.1
/
pp.131-141
/
2012
Objectives : This study was performed to investigate the effect of invasive laser acupuncture treatment at Liver Brook (LR2) acupoint and Liver Sea (LR8) acupoint on liver damage induced by D-galactosamine (D-GalN) in rats Methods : Liver damage was induced by D-GalN. The experimental rats were divided into two groups (control group, Low Level Laser Treatment (LLLT) group). Control groups were classified into small groups. Intact group had no liver damage and no treatment. D-GalN group was induced liver damage induced by D-GalN and not treated. LLLT group were induced liver damage induced by D-GalN and then treated at the LR2 or LR8 acupoint with 532, 658, 904 nm invasive laser acupuncture. The treatment was carried out three days at a time for 15days at both acupoints. To examine mechanism of the effect of invasive laser acupuncture, we measured the contents of ASP, ALT, ALP, TBIL in serum, CBC in blood and SOD in liver tissue. Results : The change of body weight increased in all groups. That change was AST and ALP, the AST activity decreased significantly compared with the control groups and decreased by 532 nm and 904 nm both LLLT groups. But ALP increased at LR8 acupoint by 658 nm. TBIL level significantly decreased in all LLLT groups. The SOD of LLLT groups increased in the liver tissue of rats compared to the control groups. SOD activity indicated that LLLT can help cellular defense mechanism by preventing scavenging hydrogen peroxide. In the change of WBC, it was increased in D-GalN Control group compared to intact group and LLLT groups. Conclusions : These results suggested that invasive laser acupuncture treatment at LR2 or LR8 acupoint reduced activation of hepatic enzyme and damage of liver tissue. Thus, the effect of invasive laser acupuncture was nearly identical to the way of the traditional acupuncture for the treatment of hepatocytotoxicity.
Previous studies have shown that bone marrow mesenchymal stromal cell (MSC) transplantation significantly improves the recovery of neurological function in a rat model of intracerebral hemorrhage. Potential repair mechanisms involve anti-inflammation, anti-apoptosis and angiogenesis. However, few studies have focused on the effects of MSCs on inducible nitric oxide synthase (iNOS) expression and subsequent peroxynitrite formation after hypertensive intracerebral hemorrhage (HICH). In this study, MSCs were transplanted intracerebrally into rats 6 hours after HICH. The modified neurological severity score and the modified limb placing test were used to measure behavioral outcomes. Blood-brain barrier disruption and neuronal loss were measured by zonula occludens-1 (ZO-1) and neuronal nucleus (NeuN) expression, respectively. Concomitant edema formation was evaluated by H&E staining and brain water content. The effect of MSCs treatment on neuroinflammation was analyzed by immunohistochemical analysis or polymerase chain reaction of CD68, Iba1, iNOS expression and subsequent peroxynitrite formation, and by an enzyme-linked immunosorbent assay of pro-inflammatory factors (IL-$1{\beta}$ and TNF-${\alpha}$). The MSCs-treated HICH group showed better performance on behavioral scores and lower brain water content compared to controls. Moreover, the MSC injection increased NeuN and ZO-1 expression measured by immunochemistry/immunofluorescence. Furthermore, MSCs reduced not only levels of CD68, Iba1 and pro-inflammatory factors, but it also inhibited iNOS expression and peroxynitrite formation in perihematomal regions. The results suggest that intracerebral administration of MSCs accelerates neurological function recovery in HICH rats. This may result from the ability of MSCs to suppress inflammation, at least in part, by inhibiting iNOS expression and subsequent peroxynitrite formation.
Journal of the Korean Society of Food Science and Nutrition
/
v.26
no.4
/
pp.689-696
/
1997
The effects of Aralia canescens and Phellodendron amurense(AP) extracts on the experimental diabetes in ICR mice were investigated. 96male ICR mice were induced diabetes mellitus by intrape-ritoneal streptozotocin injection(75mg/kg B.W.) and divided into two injection groups which are 5 day injection and 10 day injection group. Then, each injection group was subdivided into 8 groups of 6 animals repspectively. CIC served as control and CI1, CI2 and CI3 were treated with 50, 150, 250mg/kg B.W. of AP extracts powder in 0.9% NaCl solution. Animals of groups DIC, DI1, DI2 and DI3 were strepto-zotocin-induced diabetes. DIC served as diabetic control and the rest groups received 50, 150, 250mg/kg B.W of AP extracts powder in saline solution respectively. The body weight, liver and kiney weight changes and blood levels of glucose, cholesterol and triglyceride were measured. Thiobarbituric acid reactive substance(TBARS), and glutathione reductase(GR) and glutathione peroxidase(GPx) activities were also measured for determining antioxidant effects. AP extracts increased the body weight in diabetic groups. The liver and kidney weight/100g B.W. in DIC group were greater than those of normal ICR group but after AP extracts injection, liver and kidney weight were decreased significantly. These effects were more efficient at 10 days injection group. The total, LDL, VLDL cholesterol and triglyceride levels were significantly higher in DIC group and the extent of decrement responded to AP injection dose. The contents of TBARS and antioxidant enzyme activities were relatively decreased after AP extracts injection. These results suggest that the intraperitoneally administered AP extracts may have not only hypoglycemic effect but act as antioxidants by reducing lipid peroxidation.
Purpose: Hrd1 has recently emerged as a critical regulator of B-cells in autoimmune diseases. However, its role in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) remains largely unexplored. This study aimed to examine Hrd1 expression and B-cell accumulation and their possible roles in CRSwNP. Methods: Quantitative real-time polymerase chain reaction, immunohistochemistry, enzyme-linked immunosorbent assay and Western blotting were used to assess gene and protein expression in nasal tissue extracts. Cells isolated from nasal tissues and peripheral blood mononuclear cells were characterized by flow cytometry. Local antibody production was measured in tissue extracts with a Bio-Plex assay. Additionally, changes in Hrd1 expression in response to specific inflammatory stimuli were measured in cultured dispersed polyp cells. Results: Nasal polyps (NPs) from patients with eosinophilic CRSwNP (ECRS) had increased levels of Hrd1, B-cells and plasma cells compared with NPs from patients with non-eosinophilic CRSwNP (non-ECRS) or other control subjects (P < 0.05). The average Hrd1 levels in B-cells in NPs from ECRS patients were significantly higher than those from non-ECRS patients and control subjects (P < 0.05). NPs also contained significantly increased levels of several antibody isotypes compared with normal controls (P < 0.05). Interestingly, Hrd1 expression in cultured polyp cells from ECRS patients, but not non-ECRS patients, was significantly increased by interleukin-$1{\beta}$, lipopolysaccharide and Poly(I:C) stimulation, and inhibited by dexamethasone treatment (P < 0.05). Conclusions: Differential Hrd1 expression and B-cell accumulation between the ECRS and non-ECRS subsets suggests that they can exhibit distinct pathogenic mechanisms and play important roles in NP.
Particulate matter (PM) causes oxidative stress and can rapidly diffuse from the lung to the blood and accumulate in the liver when inhaled. Natural antioxidants can be used to protect against oxidative stress caused by PM. Sargassum horneri, a brown seaweed, possesses antioxidative activity and is a good source of functional foods. Therefore, this study investigated the antioxidant potential of S. horneri extract (SHE) in the livers of PM-induced asthmatic mice. PM inhalation triggered lipid peroxidation and oxidative stress, and SHE treatment attenuated malondialdehyde in the liver of mice with PM-induced asthma. Furthermore, SHE mitigated the increase in catalase activity. Importantly, SHE reduced the activity of 8-oxoguanine glycosylase (OGG1), a DNA repair enzyme. These results suggest that SHE has antioxidant potential for moderating PM-induced oxidative stress and DNA damage in the liver of asthmatic mice.
Lee, Se Hui;Lee, Jin A;Shin, Mi-Rae;Lee, Ji Hye;Roh, Seong-Soo
The Journal of Internal Korean Medicine
/
v.42
no.1
/
pp.11-24
/
2021
Objective: Chronic reflux esophagitis (CRE), characterized by esophageal mucosa ulcer, is caused by continuous backflow of gastric acid and consequent inflammation due to unstable gastroesophageal sphincter. The aim of the present study was to clarify the effect of an Arecae Semen and Coptidis Rhizoma mixture (AC-mix) on CRE. Methods: CRE was surgically induced in SD rats with three experimental groups used: normal; CRE control; and CRE treatment (200 mg/kg AC-mix). Blood and esophageal tissue were collected after two weeks of drug administration. The anti-oxidant activity of the AC-mix was measured by total polyphenol and total flavonoid contents as well as by radical scavenging activity with protein levels evaluated using western blotting. Results: CRE damage to the esophageal mucosa was significantly reduced in the AC-mix group as compared with the controls, and administration of the AC-mix was seen to inhibit NF-κBp65 activity. Consequently, the inactivation of NF-κBp65 significantly inhibited inflammatory mediators such as COX-2 and iNOS. Moreover, the anti-oxidant enzyme HO-1 significantly increased through activation of the Nrf2-Keap1 pathway. Matrix metalloproteinase-2 (MMP-2), which can break down collagen from the basement membrane and extracellular matrix, was decreased following AC-mix treatment, and elevated levels of MMP-2 were regulated by its tissue inhibitor. Conclusions: These results show that AC-mix can alleviate esophageal mucosa ulcer though inhibition of the NF-κBp65 inflammatory pathway and enhancement of the anti-oxidant Nrf2-Keap1 pathway.
Choi, Eun Wha;Lee, Hee Woo;Lee, Jun Sik;Kim, Il Yong;Shin, Jae Hoon;Seong, Je Kyung
BMB Reports
/
v.52
no.4
/
pp.289-294
/
2019
The present study evaluated the role of AHNAK in Bartonella henselae infection. Mice were intraperitoneally inoculated with $2{\times}10^8$ colony-forming units of B. henselae Houston-1 on day 0 and subsequently on day 10. Blood and tissue samples of the mice were collected 8 days after the final B. henselae injection. B. henselae infection in the liver of Ahnak-knockout and wild-type mice was confirmed by performing polymerase chain reaction, with Bartonella adhesion A as a marker. The proportion of B. henselae-infected cells increased in the liver of the Ahnak-knockout mice. Granulomatous lesions, inflammatory cytokine levels, and liver enzyme levels were also higher in the liver of the Ahnak-knockout mice than in the liver of the wild-type mice, indicating that Ahnak deletion accelerated B. henselae infection. The proportion of CD4+interferon-${\gamma}$ ($IFN-{\gamma}^+$) and $CD4^+$ interleukin $(IL)-4^+$ cells was significantly lower in the B. henselae-infected Ahnak-knockout mice than in the B. henselae-infected wild-type mice. In vitro stimulation with B. henselae significantly increased $IFN-{\gamma}$ and IL-4 secretion in the splenocytes obtained from the B. henselae-infected wild-type mice, but did not increase $IFN-{\gamma}$ and IL-4 secretion in the splenocytes obtained from the B. henselae-infected Ahnak-KO mice. In contrast, $IL-1{\alpha}$, $IL-1{\beta}$, IL-6, IL-10, RANTES, and tumor necrosis $factor-{\alpha}$ secretion was significantly elevated in the splenocytes obtained from both B. henselae-infected wild-type and Ahnak-knockout mice. These results indicate that Ahnak deletion promotes B. henselae infection. Impaired $IFN-{\gamma}$ and IL-4 secretion in the Ahnak-knockout mice suggests the impairment of Th1 and Th2 immunity in these mice.
Jung, Su Min;Seol, Young Hyun;Chun, Ka Yoon;Park, Min Ha;Liu, Yi;Kang, Seok Yong;Park, Yong-Ki;Jung, Hyo Won
Journal of Korean Medicine for Obesity Research
/
v.20
no.2
/
pp.69-77
/
2020
Objectives: In this study, we investigated the antiobesity and antidiabetic effects of polyherbal extract, DM2 consisting of Atractylodis Rhizoma, Anemarrhenae Rhizoma, Cinnamomi Cortex, and Moutan Radicles Cortex in high fat diet-induced obesity mice. Methods: DM2 extract was prepared with a hot water. Six-week-old male C57BL/6N mice were fed a high-fat diet (HFD) for 8 weeks and then administrated with DM2 extract (500 mg/kg, p.o.) for 4 weeks. The changes of physiological markers, body weight (BW), food and water intakes, and the levels of fasting blood glucose (FBG) were measured once a week for 4 weeks in mice. The the serum levels of glucose, insulin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol (T-CHO), triglyceride, and low density lipoprotein cholesterol in sera were measured in mice using autometic chemical analyzer and enzyme linked immunosorbant assay. We also observed the histological changes of liver and pancreatic tissues with Hematoxylin & Eosin staining. Results: In physiological change, the increases of BW, calorie intake, and FBG in HFD-induced obese mice were significantly decreased after administration of DM2 extract for 4 weeks. The decrease of water intake was significantly increased in DM2 extract-administrated mice. In serological change, the administration of DM2 extract in obesity mice was significantly decreased the serum levels of glucose, insulin, T-CHO, AST, and ALT levels. We also found that DM2 extract inhibited the increase of lipid droplets in liver and the structural destruction of pancreatic tissues in obesity mice. Conclusion: Our study demonstrated that DM2 extract has antiobesity antidiabetic effects with body weight loss, decrease of glucose and insulin levels, and lipid accumulation on liver tissue.
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