Effects of telmisartan on improving leptin resistance and inhibiting hepatic fibrosis in rats with non-alcoholic fatty liver disease

Zhang, Qiu-Zan; Liu, Yingli; Wang, Yanrong; Fu, Ling; Zhang, Jing; Xiu-ru, Wang; Wang, Bangmao

doi:10.3892/etm.2017.4809

Cited by 17 publications

(7 citation statements)

References 36 publications

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“…The mean value of NFS was significantly increased in Group I while it remained stable in Group II, which indicated that telmisartan prevented the progression of liver fibrosis. This observation confirmed previous studies that showed telmisartan had antifibrotic effect (15,33,34). The antifibrotic effect of telmisartan is associated with suppression of inflammasome maturation by evidence of a significant decrease of serum levels of IL-1β and Il-18.…”

Section: Discussionsupporting

confidence: 93%

“…It suppressed the expressions of C-reactive protein (CRP) IL-1β, IL-6, and TNF-α in the experimental animal model of acute colitis and acute myocardial infarction (13,14). Telmisartan reduced the fibrosis liver score in rats fed with high fat diet for three months, which represented an animal model of NAFLD, by suppressing the expression of leptin in the liver (15). In the murine NASH model, telmisartan delay the progression of steatohepatitis by complex mechanisms including anti-inflammatory (as it suppressed macrophage infiltration into the liver), and anti-adiposity like effect (16).…”

Section: Introductionmentioning

confidence: 99%

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Telmisartan improves the metabolic, hematological and inflammasome indices in non-alcoholic fatty liver infiltration: A pilot open-label placebo-controlled study

2019

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Telmisartan improves the metabolic, hematological and inflammasome indices in non-alcoholic fatty liver infiltration: A pilot open-label placebo-controlled study

2019

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“…Conversely, HF animals treated with losartan or telmisartan benefited from AT1r blockade, as they favored the ACE2/MASr axis over the ACE1/AT1r axis, which has been previously associated with the amelioration of glucose intolerance, hepatic inflammation, and prevention of steatosis and fibrosis[8,15,20]. The RAS modulation by telmisartan can explain previous beneficial effects on the livers of an animal model of hepatic fibrosis[27] and in human with steatohepatitis[28], without side effects. Although the HF diet did not induce fibrosis, our results show that the AT1R blockade reduced PLIN 2 expression and hepatic triacylglycerol levels, both of which are strongly correlated with reduced hepatic steatosis[11,29].…”

Section: Discussionmentioning

confidence: 99%

Beneficial effects of losartan or telmisartan on the local hepatic renin-angiotensin system to counter obesity in an experimental model

Graus-Nunes¹,

Santos²,

Marinho³

et al. 2019

WJH

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BACKGROUND Obesity has been associated with hepatic overexpression of the renin-angiotensin system (RAS). AIM To evaluate the action of two angiotensin II (ANGII) receptor blockers (losartan or telmisartan) on the modulation of local hepatic RAS and the resulting metabolic effects in a diet-induced obesity murine model. METHODS Twenty C57BL/6 mice were randomly divided into two nutritional groups for 10 wk: control group (C, n = 5, 10% of energy as fat) or high-fat group (HF, n = 15, 50% of energy as fat). After treatment started, the HF group was randomly divided into three groups: untreated HF group ( n = 5), HF treated with losartan (HFL, n = 5) and HF treated with telmisartan (HFT, n = 5). The treatments lasted for 5 wk, and the dose was 10 mg/kg body mass. RESULTS HF diet induced body mass gain (+28%, P < 0.0001), insulin resistance (+69%, P = 0.0079), high hepatic triacylglycerol (+127%, P = 0.0004), and overexpression of intrahepatic angiotensin-converting enzyme (ACE) 1/ ANGII type 1 receptor (AT1r) (+569.02% and +141.40%, respectively, P < 0.0001). The HFL and HFT groups showed higher ACE2/rMAS gene expression compared to the HF group (ACE2: +465.57%, P = 0.0002 for HFL and +345.17%, P = 0.0049 for HFT; rMAS: +711.39%, P < 0.0001 for HFL and +539.75%, P < 0.0001 for HFT), followed by reduced insulin/glucose ratio (-30% for HFL and -33% for HFT, P = 0.0181), hepatic triacylglycerol levels (-28%, P = 0.0381 for HFL; and -45%, P = 0.0010 for HFT, and Plin2 expression. CONCLUSION Modulation of the intrahepatic RAS, with favored involvement of the ACE2/rMAS axis over the ACE1/AT1r axis after losartan or telmisartan treatments, caused hepatic and metabolic beneficial effects as demonstrated by reduced hepatic triacylglycerol levels coupled with reduced PLIN 2 expression and improved glycemic control.

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“…Polyene phosphatidylcholine (PPC) is a hepatoprotective agent, which has been widely used to treat various types of hepatopathy such as viral hepatitis, liver damage or nonalcoholic steatohepatitis [25][26][27][28]. The drug can be extracted from soy and rich in polyunsaturated fatty acids [29].…”

Section: Introductionmentioning

confidence: 99%

Polyene Phosphatidylcholine Interacting with TLR-2 Prevents the Synovial Inflammation via Inactivation of MAPK and NF-κB Pathways

et al. 2022

Inflammation

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Rheumatoid arthritis (RA) is a chronic autoimmune joint disease that causes cartilage and bone damage or even disability, seriously endangering human health. Chronic synovial in ammation has been shown to play a vital role in the disease sustainability. Therefore, down-regulation of synovial in ammation is considered to be an effective discipline for RA therapy. Polyene phosphatidylcholine (PPC) is a hepatoprotective agent, which was observed to inhibit in ammation in macrophages and prevent collagen-induced arthritis (CIA) of rats in our previous study. However, the underlying mechanism remains unclear. The present study further reported that PPC can inhibit the synovial in ammation. In lipopolysaccharide (LPS)-stimulated primary synovial broblasts (SFs) of mice, PPC signi cantly decreased pro-in ammatory cytokines production while increasing anti-in ammatory cytokines level. In this process, PPC down-regulated the expression of TLR-2 and their downstream signaling molecules such as MyD88, p-ERK1/2, p-JNK1/2, p-P38 in the MAPK pathway and p-IκBα and NF-κB-p65 in NF-kB pathway. Moreover, the inhibitory effect of PPC on the above molecules and cytokines was weakened after the use of TLR-2 agonist Pam3CSK4. However, PPC lost its anti-in ammatory effect and showed an activation of MAPK and NF-kB pathways in the TLR-2 -/primary SFs after exposure to LPS. Furthermore, these results were con rmed in the SFs from the CIA mouse ex vivo. Collectively, this study demonstrated that PPC can alleviate synovial in ammation through TLR-2 mediated MAPK and NF-κB pathways, which can be proposed to be a potential drug candidate for RA therapy.

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Effects of telmisartan on improving leptin resistance and inhibiting hepatic fibrosis in rats with non-alcoholic fatty liver disease

Cited by 17 publications

References 36 publications

Telmisartan improves the metabolic, hematological and inflammasome indices in non-alcoholic fatty liver infiltration: A pilot open-label placebo-controlled study

Telmisartan improves the metabolic, hematological and inflammasome indices in non-alcoholic fatty liver infiltration: A pilot open-label placebo-controlled study

Beneficial effects of losartan or telmisartan on the local hepatic renin-angiotensin system to counter obesity in an experimental model

Polyene Phosphatidylcholine Interacting with TLR-2 Prevents the Synovial Inflammation via Inactivation of MAPK and NF-κB Pathways

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