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Yue-Min Nan,
Ling-Bo Kong,
Wei-Guang Ren,
Rong-Qi Wang,
Jing-Hua Du,
Wen-Cong Li,
Su-Xian Zhao,
Yu-Guo Zhang, Wen-Juan Wu,
Hai-Ling Di,
Ya Li,
Jun Yu
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ABSTRACT: BACKGROUND: Peroxisome proliferator activated receptor alpha (PPARalpha) ameliorates ethanol induced hepatic steatohepatitis. However, its role in alcoholic liver fibrosis has not been fully clarified. The aim of this study was to elucidate the effect and the molecular basis of PPARalpha in ethanol induced liver fibrosis in mice. METHODS: C57BL/6J mice were fed with 4% ethanol-containing Lieber-DeCarli liquid diet for eight weeks, and intraperitoneal injected with 5% carbon tetrachloride (CCl4) for the last four weeks to induce alcoholic liver fibrosis. PPARalpha agonist WY14643 was administered to mice during the last couple of weeks. The effects of PPARalpha induction on liver histology, activation of hepatic stellate cells (HSCs), as well as hepatic expression of inflammatory and fibrogenic factors were assessed. RESULTS: The ethanol plus CCl4 treated mice exhibited progressive liver injury including piecemeal necrosis of hepatocytes, severe inflammatory cells infiltration and bridging fibrosis. This was accompanied by down-regulated hepatic expression of PPARalpha and the protective cytokines adiponectin, heme oxygenase-1 and interleukin-10. Additionally, up-regulation of the proinflammatory cytokine tumor necrosis factor-alpha, as well as the profibrogenic genes osteopontin, transforming growth factor-beta 1, visfatin, phosphatidylinositol 3-kinase, matrix metalloproteinase-2 (MMP-2) and MMP-9 was observed. WY14643 treatment restored expression of cytokines altered by ethanol plus CCl4 treatment and concomitantly ameliorated the liver injury. CONCLUSIONS: The present study provides evidence for the protective role of PPARalpha induction in ameliorating ethanol mediated fibrosis through mediation of inflammatory and fibrogenic factors.
Lipids in Health and Disease 02/2013; 12(1):11. · 2.17 Impact Factor
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Yan-Hong Jia,
Rong-Qi Wang,
Hong-Mei Mi,
Ling-Bo Kong,
Wei-Guang Ren,
Wen-Cong Li,
Su-Xian Zhao,
Yu-Guo Zhang, Wen-Juan Wu,
Yue-Min Nan,
Jun Yu
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ABSTRACT: Fuzheng Huayu recipe (FZHY), a compound of Chinese herbal medicine, was reported to improve liver function and fibrosis in patients with hepatitis B virus infection. However, its effect on nutritional fibrosing steatohepatitis is unclear. We aimed to elucidate the role and molecular mechanism of FZHY on this disorder in mice.
C57BL/6 J mice were fed with methionine-choline deficient (MCD) diet for 8 weeks to induce fibrosing steatohepatitis. FZHY and/or heme oxygenase-1 (HO-1) chemical inducer (hemin) were administered to mice, respectively. The effect of FZHY was assessed by comparing the severity of hepatic injury, levels of hepatic lipid peroxides, activation of hepatic stellate cells (HSCs) and the expression of oxidative stress, inflammatory and fibrogenic related genes.
Mice fed with MCD diet for 8 weeks showed severe hepatic injury including hepatic steatosis, necro-inflammation and fibrosis. Administration of FZHY or hemin significantly lowered serum levels of alanine aminotransferase, aspartate aminotransferase, reduced hepatic oxidative stress and ameliorated hepatic inflammation and fibrosis. An additive effect was observed in mice fed MCD supplemented with FZHY or/and hemin. These effects were associated with down-regulation of pro-oxidative stress gene cytochrome P450 2E1, up-regulation of anti-oxidative gene HO-1; suppression of pro-inflammation genes tumor necrosis factor alpha and interleukin-6; and inhibition of pro-fibrotic genes including α-smooth muscle actin, transforming growth factor beta 1, collagen type I (Col-1) and Col-3.
Our study demonstrated the protective role of FZHY in ameliorating nutritional fibrosing steatohepatitis. The effect was mediated through regulating key genes related to oxidative stress, inflammation and fibrogenesis.
Lipids in Health and Disease 03/2012; 11(1):45. · 2.17 Impact Factor
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ABSTRACT: To explore the relationship between the causes and length of posterior malleolar fragment and treatment strategies of adult patients with three types of ankle joint injury.
The investigators recruited 233 cases of type C injury, 35 cases of type B injury and 91 cases of type A injury. Type A injury referred to simple ankle joint fracture with the involvement of posterior malleolar fragment. Type B injury tibial shaft fracture with ipsilateral ankle joint fracture. And posterior malleolar fracture line was the continuity of tibial shaft fracture line. Type C injury appeared similar to Type B injury, but tibial and malleolar fracture lines were not continued. The ratio between the length of posterior malleolar articular and the total length of articular surface was calculated in theses three types of injuries in sagittal CT scan slice. Different treatment regimens were used to manage the posterior malleolar fractures. And visual analogue score (VAS) was introduced to assess the therapeutic outcomes.
The ratio between the length of posterior malleolar articular and the total length of articular surface decreased from Type A to Type C (χ(2) = 187.453, P = 0.0000). The ratio was (34 ± 15)% for Type A, (30 ± 9)% for Type B and (12 ± 10)% for Type C. A follow-up study was performed in Type A injury (n = 58), Type B injury (n = 31) and Type C injury (n = 167) at 12 months. According to VAS score, there was no significant difference between the patients undergoing fixation and not (all P > 0.05).
Different causes of posterior malleolar fracture results in different sizes of posterior malleolar fragment and strategies of treatment. The anatomic reduction of posterior malleolar fragment remains a key aspect of achieving satisfactory outcomes in all kinds of injury.
Zhonghua yi xue za zhi 11/2011; 91(41):2917-9.
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ABSTRACT: Our previous study indicated that the death receptor Fas played a key role on hepatocyte apoptosis in nutritional steatohepatitis in mice. This study aimed to explore whether Fas mutation accelerated hepatic steatosis and inflammatory infiltration in methionine-choline deficient (MCD) diet feeding mice.
Mice homozygous for the lymphoproliferation spontaneous mutation (C57BL/6J-Faslpr) and wild type C57BL/6J mice were fed with MCD diet for three weeks to induce non-alcoholic steatohepatitis (NASH). Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG) and total cholesterol (TC) levels were detected by an Olympus AU5400 automatic chemical analyzer. The role of Fas gene mutation on NASH was assessed by comparing the severity of hepatic steatosis and inflammation in the liver sections, the mRNA and protein expressions of hepatic inflammatory and fibrogenesis related factors, proliferating cell nuclear antigen (PCNA) and transforming growth factor beta 1 (TGFb1).
The serum ALT levels of the wild type and Faslpr mice fed with MCD were significant higher than that of the control mice (126.33+/-10.50 U/L vs (25.00+/-10.14) U/L, (160.33+/-48.29) U/L vs (18.33+/-9.08) U/L, with the LSD-t value 12.02, 5.08 respectively, the P value<0.001, 0.007 respectively. The serum ALT levels showed no significant difference between the Faslpr and wild type mice fed with MCD, with the LSD-t value 1.19, the P value 0.229. The serum AST, TG and TC levels showed neithere significant difference among the four groups. MCD diet induced hepatic steatosis and inflammatory infiltration in both of the wild type and Faslpr mice. Especially, severer hepatic injury was observed in Faslpr mice as compared with wild type mice. The mRNA expression levels of cell proliferation factor PCNA and fibrogenesis growth factor TGF b1 in wild type mice fed with MCD were significantly higher than that of the control mice (2.84+/-0.73, 2.77+/-0.54 vs 1.31+/-0.18, 0.89+/-0.18), with the LSD-t value 4.99, 8.08 respectively, the P value 0.001, <0.001 respectively. The mRNA expression levels of PCNA and TGFb1 in Faslpr mice fed with MCD were significantly higher than that of the Faslpr control mice and the wild type mice fed with MCD (5.57+/-1.13, 5.73+/-0.89 vs 1.04+/-0.16, 0.85+/-0.11 and 2.84+/-0.73, 2.77+/-0.54), with the LSD-t value 10.15, 13.19 and 5.33, 6.91 respectively, the P value<0.001. The protein expressions levels of PCNA and TGFb1 were concordant with the mRNA.
Faslpr promoted hepatic steatosis and inflammatory infiltration in mice fed with MCD diet, which might associated with excessive release of cell proliferative, inflammatory and fibrogenesis factors.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 09/2011; 19(9):653-7.
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ABSTRACT: Heme oxygenase-1 (HO-1), an antioxidant defense enzyme, has been shown to protect against oxidant-induced liver injury. However, its role on liver fibrosis remains unclear. This study aims to elucidate the effect and the mechanism of HO-1 in nutritional fibrosing steatohepatitis in mice.
Male C57BL/6J mice were fed with a methionine-choline deficient (MCD) diet for eight weeks to induce hepatic fibrosis. HO-1 chemical inducer (hemin), HO-1 chemical inhibitor zinc protoporphyrin IX (ZnPP-IX) and/or adenovirus carrying HO-1 gene (Ad-HO-1) were administered to mice, respectively. Liver injury was assessed by serum ALT, AST levels and histological examination; hepatic lipid peroxides levels were determined; the expression levels of several fibrogenic related genes were assayed by real-time quantitative PCR and Western blot.
MCD feeding mice showed progressive hepatic injury including hepatic steatosis, inflammatory infiltration and fibrosis. Induction of HO-1 by hemin or Ad-HO-1 significantly attenuated the severity of liver injury. This effect was associated with the up-regulation of HO-1, reduction of hepatic lipid peroxides levels, down-regulation of inflammatory factors tumor necrosis factor-alpha, interleukin-6 and suppressor of cytokine signaling-1 as well as the pro-fibrotic genes alpha-smooth muscle actin, transforming growth factor-β1, matrix metallopeptidase-2 and matrix metallopeptidase-9. A contrary effect was observed in mice treated with ZnPP-IX.
The present study provided the evidence for the protective role of HO-1 in ameliorating MCD diet-induced fibrosing steatohepatitis. Modulation of HO-1 expression might serve as a therapeutic approach for fibrotic steatohepatitis.
Lipids in Health and Disease 02/2011; 10:31. · 2.17 Impact Factor
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ABSTRACT: The pathogenesis of non-alcoholic steatohepatitis is still unclear. We have demonstrated previously that peroxisome proliferator activated receptor gamma (PPARγ) ligand protects against inflammation and fibrogenesis in experimental non-alcoholic steatohepatitis. We aim to elucidate the effect and the mechanism of PPARγ itself on nutritional fibrotic steatohepatitis in mice.
C57BL/6J mice were fed with methionine-choline deficient (MCD) diet for 8 weeks to induce fibrotic steatohepatitis. Mice fed the MCD diet were treated with adenovirus carrying PPARγ (Ad-PPARγ), Ad-PPARγ plus PPARγ agonist rosiglitazone, or PPARγ antagonist 2-chloro-5-nitrobenzaniliden (GW9662), respectively. The effects of up-regulation of PPARγ in the presence or absence of its agonist/or antagonist were assessed by comparing the severity of hepatic injury, activation of hepatic stellate cells and the expression of adiponectin, heme oxygenase-1, and fibrogenic related genes.
Mice fed with MCD diet for 8 weeks showed severe hepatic injury including hepatic steatosis, inflammatory infiltration, and fibrosis. Administration of Ad-PPARγ significantly lowered serum alanine aminotransferase level and ameliorated hepatic steatosis, necroinflammation, and fibrosis. These effects were associated with enhanced expression of PPARγ, up-regulated expression of adiponectin and heme oxygenase-1, and down-regulated expression of tumor necrosis factor alpha, interleukin-6, α-smooth muscle actin, transforming growth factor beta 1, matrix metallopeptidase-2, and -9. Administration of GW9662 promoted the severity of liver histology.
The present study provided evidences for the protective role of overexpressing PPARγ in ameliorating hepatic fibrosing steatohepatitis in mice. Modulation of PPARγ expression might serve as a therapeutic approach for fibrotic steatohepatitis.
Scandinavian journal of gastroenterology 10/2010; 46(3):358-69. · 2.08 Impact Factor
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ABSTRACT: To investigate the potential role of heme oxygenase-1 on preventing non-alcoholic steatohepatitis (NASH) in mice.
Experimental models of NASH were established by feeding male C57BL/6J mice with choline-methionine deficient diet (MCD) for four weeks. Control animals were fed with choline-methionine supplemented diet. The treatment groups were fed with MCD diet combined with HO-1 inducer hemin or inhibitor zinc protoporphyrin IX (ZnPP-IX). Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were tested by enzymic method with automatic biochemistry analyzer. The degree of hepatic steatosis, inflammation and fibrosis were examined under HE staining. The hepatic mRNA and protein expressions of HO-1, TNFalpha and IL-6 were analyzed by RT-PCR and Western blot respectively. MCD fed mice showed increased serum ALT and AST levels and moderate to severe hepatic steatosis with inflammatory infiltration, hepatic spot or focal necrosis, light portal and sinus hepaticus fibrosis in the liver sections, which associated with enhanced expression of HO-1, TNFalpha and IL-6 mRNA and protein (1.13+/-0.11, 1.74+/-0.05; 0.20+/-0.01, 1.92+/-0.10; 0.58+/-0.02, 2.06+/-0.05 vs 0.43+/-0.02, 0.75+/-0.05; 0.08+/-0.00, 0.59+/-0.02; 0.22+/-0.01, 0.91+/-0.02). Administration of hemin significantly decreased serum ALT and AST levels and attenuated hepatic steatosis and necroinflammation which associated with up-regulation of antioxidative gene HO-1 and down-regulation of pro-inflammatory cytokines TNFalpha and IL-6 (P < 0.01). A contrary effect on serum aminotransferase levels and liver histopathology was observed in mice injected with ZnPP-IX (P < 0.01).
The effect was associated with suppressed HO-1 expression and increased TNFaLPHA and IL-6 expression. The data provided a biochemical, morphological and molecular biological evidence for the protective role of HO-1 in ameliorating hepatic steatosis, necroinflammation in experimental nutritional steatohepatitis.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 09/2010; 18(9):680-4.
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ABSTRACT: To investigate retrospectively the adult metatarsal fractures within last five years and analyze their epidemiological characteristics.
The X-ray films taken from January 1, 2003 to December 31, 2007 at department of radiology of Hebei provincial orthopedic hospital were reviewed to screen and classify according to OTA fracture comprehensive classification method. The epidemiological characteristics of adult metatarsal fractures were summarized and analyzed.
A total of 1949 adult metatarsal fractures were included. The single and multiple types were 1465 and 484 respectively. The 31-50-yr age group was the largest one with 45.26% of the patients. The fifth metatarsal fracture was the most common metatarsal fracture accounting for 42.45% of the total; 58.37% of metatarsal fractures occurred in proximal metaphysis; 87.61% of multiple metatarsal fractures occurred in adjacent metatarsals; 81-A1 group fracture was the most common metatarsal fracture accounting for 35.42% of the total.
Epidemiological studies of metatarsal fracture offer aids in the diagnosis and treatment of metatarsal fractures.
Zhonghua yi xue za zhi 01/2010; 90(1):15-8.
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ABSTRACT: Hepatic oxidative stress plays a key role in the development of non-alcoholic steatohepatitis (NASH). However, the protective effects of antioxidants on NASH are largely unknown. The aim of this study was to elucidate the effect and mechanism of antioxidants on NASH in mice.
C57BL6/J mice were fed a methionine-choline-deficient (MCD) diet for 10 days or 3 weeks to induce steatohepatitis. Antioxidants (vitamin E, ABT, or vitamin E plus ABT) were supplemented in mice fed a MCD diet, respectively. The effect of antioxidants on oxidative stress and apoptosis was assessed, and activation of adiponectin and expressions of inflammatory factors, apoptosis-related genes, and fibrosis-related genes were assayed.
MCD feeding in mice showed increasing serum alanine aminotransferase (ALAT) and aspartate aminotransferase (ASAT) levels, and progressive hepatic injury including hepatic steatosis and inflammatory infiltration. Administration of antioxidants vitamin E and/or ABT significantly lowered serum ALAT and ASAT levels (p<0.001) and ameliorated hepatic steatosis and necroinflammation. These effects were associated with repressed hepatic lipid peroxides through reducing hepatic MDA content and enhancing hepatic superoxide dismutase (SOD) activity; down-regulated inflammatory factor COX-2, lowered activity of NF-kappaB, up-regulated anti-apoptotic gene Bcl-2, and down-regulated pro-apoptotic gene Bax suppressed expression of the fibrotic genes TGF-beta1 and MMP2. Moreover, expression of the anti-inflammatory factor adiponectin was also induced by vitamin E or ABT. A combination of vitamin E and ABT showed an additive effect on preventing liver injury.
The present study provides morphological and molecular biological evidence for the protective role of the antioxidant vitamins E and ABT in ameliorating oxidative stress, hepatic apoptosis, and necroinflammation in experimental nutritional steatohepatitis.
Scandinavian journal of gastroenterology 07/2009; 44(9):1121-31. · 2.08 Impact Factor
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ABSTRACT: Currently, no agent has been confirmed as preventing the fibrosing progression of non-alcoholic steatohepatitis (NASH). In this study, rosiglitazone was used in the clinical treatment of insulin resistance in patients with type 2 diabetes mellitus. However, its protective effect on non-alcoholic fibrosing steatohepatitis is not clear. The study aimed to elucidate the effect and the mechanism of rosiglitazone in inhibiting nutrition-related fibrosis in mice.
C57BL6/J mice were fed a high fat, methionine-choline deficient (MCD) diet for 8 weeks to induce hepatic fibrosis, and rosiglitazone was given in the treated group. The effect of rosiglitazone was assessed by comparing the severity of hepatic fibrosis in liver sections, the activation of hepatic stellate cells (HSCs) and the expression of TGF-beta1 and connective tissue growth factor (CTGF).
At week 8, MCD-diet-induced fibrosing NASH models showed increased serum ALT and AST levels, severe hepatic steatosis, and infiltration of inflammation and fibrosis which, associated with down-regulated PPAR gamma mRNA and protein expression, up-regulated alpha-SMA protein expression and enhanced TGF-beta1, CTGF mRNA and protein expression. Rosiglitazone significantly lowered serum ALT and AST and it reduced MCD-induced fibrosis by repressing levels of alpha-SMA protein expression and pro-fibrosis factors TGF-beta1 and CTGF. It also restored expression of PPAR gamma.
The present study provides clear morphological and molecular biological evidence of the protective role of rosiglitazone in ameliorating nutritional fibrosing steatohepatitis. Rosiglitazone may ameliorate hepatic fibrosis by activating PPAR gamma, which can inhibit HSC activation and suppress TGF-beta1 and CTGF expression.
Scandinavian journal of gastroenterology 12/2008; 44(3):358-65. · 2.08 Impact Factor
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ABSTRACT: To investigate the difference between the spiral tibial shaft fracture combined with ipsilateral posterior malleolar fracture.(TSPMF) and simple ipsilateral posterior malleolar fracture in ankle joint fracture in adults.
The sex, age, and type and mechanism of fracture of 82 patients with tibial shaft fracture associated with ankle joint fracture (TAF) and 28 patients with tibial shaft spiral fracture associated with ipsilateral posterior malleolar fracture (TSPMF) among 1685 cases of adult tibial and fibular shaft fracture and 330 patients with posterior malleolar fracture among 1871 cases of simple ankle joint fracture were analyzed.
The mean age of the 28 cases with TSPMF, 24 males and 4 females, was (41.1 +/- 11.8). The mean age of the 330 cases with simple posterior malleolar fracture, 187 males and 143 females, was (42.6 +/- 15.9). The incidence of posterior malleolar fracture in the TAF patients was 34.1% (28/82), significantly higher than that of the simple ankle joint fracture [17.6%, 330/1871, P = 0.000]. The rate of combined external malleolus and posterior malleolus in the TSPMF patients was 17.9% (5/28), significantly that in the patients with simple ankle joint fracture (73.7%, 159/330, P = 0.000). The fibular fracture line of 75.0% (21/28) of the TSPMF patients was located over the level of the lower tibiofibular ligament union, a rate significantly higher than that in the simple malleolus fracture (24.8%, 82/330, P = 0.000).
Spiral tibial shaft fracture associated with ipsilateral posterior malleolar fracture is a special kind of fracture; the cause and mechanism of TSPMF are difference from those of the ankle joint fracture.
Zhonghua yi xue za zhi 11/2008; 88(39):2775-8.
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ABSTRACT: To investigate the clinical epidemiological features of adult spiral tibial shaft fracture associated with ipsilateral posterior malleolar fracture, a special kind of fracture.
The clinical data of 1685 cases of adult tibial and fibular shaft fracture were analyzed retrospectively. The cause and mechanism of spiral tibial shaft fracture associated with ipsilateral posterior malleolar fracture were studied in detail.
The male and female ratio in adult tibial and fibular shaft fracture was 4.52:1. Most of adult tibial and fibular shaft fracture occurred in the persons aged 31 - 40 (26.0%) and type A fracture accounted for 57.7% of the cases. The male and female ratio in adult spiral tibial fracture was 2.95:1. Most of the adult spiral tibial fracture occurred in those aged 41 - 50 (32.6%). With a male and female ratio of 6:1 (24:4) and mostly occurring in the persons aged 41 - 50, spiral tibial shaft fracture associated with ipsilateral posterior malleolar fracture composed 9.7% (28/288) of total tibial fractures and 1.7% (28/1685) of total spiral tibial and fibular fractures. Missed diagnosis rate of spiral tibial shaft fracture associated with ipsilateral posterior malleolar fracture was 67.9% (19/28) in the Department of Radiology and 53.6% in the Department of Orthopedics.
With a high incidence, spiral tibial shaft fracture associated with ipsilateral posterior malleolar fracture was caused by a low energy but not an iatrogenic damage. With a high rate of missed diagnosis, the spiral tibial shaft fracture associated with ipsilateral posterior malleolar fracture should be paid more attention to clinically.
Zhonghua yi xue za zhi 09/2008; 88(31):2166-70.
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ABSTRACT: To study the role of apoptosis and the expression of apoptosis-related genes Fas ligand (FasL), Fas, caspase-3 and caspase-8 in an animal model of non-alcoholic steatohepatitis (NASH).
An experimental progressive NASH model was established by feeding male C57BL6/J mice with a high fat, methionine-choline deficient (MCD-) diet for two days, five days, ten days, three weeks and eight weeks. Control mice were fed methionine-choline supplemented (MCD+) diet. Hepatic steatosis, inflammation and fibrosis were graded by examining their H and E stained liver sections. Hepatocyte apoptosis was detected by TUNEL assay. Expressions of mRNA and protein of FasL, Fas and caspase-8 were performed by quantitative real time RT-PCR and Western blot. Caspase-3 activity assay was conducted using ApoAlert caspase-3 assay kit.
In MCD- mice, minimal hepatic steatosis was observed at day 5, and by day 10, mild steatosis with inflammatory infiltration was found. Severe steatohepatitis was noted at week 3, and fibrosis at week 8. TUNEL assay showed that apoptotic index in MCD- group was higher than that in MCD+ group at week 3 (15.59%+/-4.87% vs 5.17%+/-3.19%, P less than 0.05) and at week 8 (11.29%+/-3.22% vs 5.41%+/-1.54%, P less than 0.05). Compared to MCD+ group, the expression of FasL was dramatically increased on day 10 and in week 3 in MCD- mice both at the mRNA and protein levels (P less than 0.05 and P less than 0.01). Expression of Fas mRNA was up-regulated in weeks 3 and 8 (P less than 0.01), and expression of Fas in protein level was higher at week 8 (P less than 0.01) in MCD- group. Expression of caspase-8 significantly increased at the mRNA level at week 3 and week 8 (P less than 0.01 and P less than 0.05 respectively) and at the protein level at week 8 (P less than 0.05) in MCD- group. In all of the time points except for day 5, caspase-3 activities were significantly more enhanced in MCD- group than that in MCD+ group (P less than 0.05).
In our experimental NASH model, hepatic apoptosis was frequently detected. Increased apoptosis was probably attributable to up-regulation of apoptosis-related genes, such as FasL/Fas system, and activation of the caspase pathway. These changes may provoke hepatic apoptosis and the development of inflammation and fibrosis.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 02/2007; 15(1):41-6.
