The protection of Rhein lysinate to liver in diabetic mice induced by high-fat diet and streptozotocin

Lin, Yajun; Hu, Gang; Li, Kai‑Ji; Zhao, Yufang; Wei, Jie; Zhen, Yong‐Su

doi:10.1007/s12272-014-0423-4

Cited by 16 publications

(13 citation statements)

References 24 publications

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“…Treatment with RHL at 50 mg/kg/day, however, could improve these values. In our previous study, we reported that RHL could decrease the body weights and blood glucose levels of mice fed a high-fat diet and that had diabetes induced using STZ (Lin et al 2015). In the present study, we also observed that 25 and 50 mg/kg/day of RHL treatment could decrease blood glucose levels, and 50 mg/ kg/day of RHL treatment could also decrease body weight, compared with the KK/HlJ model group.…”

Section: Discussionsupporting

confidence: 76%

Rhein lysinate decreases inflammation and adipose infiltration in KK/HlJ diabetic mice with non-alcoholic fatty liver disease

et al. 2016

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The objective of this study was to investigate the protective effects of rhein lysinate (RHL) on the liver. Mice were divided into four groups: C57BL/J control, the KK/HlJ diabetic model, and 25 and 50 mg/kg/day RHL-treated KK/HlJ groups. The KK/HlJ diabetic mouse model was made by injecting STZ and feeding mice diabetic food. At 16 weeks, mice were sacrificed and their livers were harvested. The results indicated that compared with the C57BL/J control group, the body weights, liver weights and liver weight-to-body weight ratio were increased in KK/HlJ diabetic mice; however, these values were decreased following treatment with RHL. Compared with the C57BL/J control, KK/HlJ diabetic mice had a significantly lower level of SOD and GSH-px in their livers, but had a significantly higher level of MDA. However, these effects were ameliorated by RHL. Hepatic adipose infiltration was observed in KK/HlJ mice, but not in C57BL/J mice. RHL decreased the incidence of hepatic adipose infiltration and significantly decreased the expression of TNF-α, IL-6, NF-κB, SREBP-1c, and Fas, as well as the phosphorylation of NF-κB in the liver. In conclusion, RHL can improve hepatic function by decreasing hepatic adipose infiltration and the expression of inflammatory factors.

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Section: Discussionsupporting

confidence: 76%

Rhein lysinate decreases inflammation and adipose infiltration in KK/HlJ diabetic mice with non-alcoholic fatty liver disease

et al. 2016

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“…Considering that emodin is an anthraquinone, and many naturally occurring anthraquinones have been identified as having anti-diabetes activity (Chen et al, 2015; Lin et al, 2015; Ramos-Zavala et al, 2011; Wu et al, 2014), we wondered whether this class of compounds such as Aloe-emodin, rheochrysidin, chrysophanol and rhein, might inhibit DPP4 activity.…”

Section: Resultsmentioning

confidence: 99%

Screening of a natural compound library identifies emodin, a natural compound from Rheum palmatum Linn that inhibits DPP4

Wang

Yang

et al. 2017

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Historically, Chinese herbal medicines have been widely used in the treatment of hyperglycemia, but the mechanisms underlying their effectiveness remain largely unknown. Here, we screened a compound library primarily comprised of natural compounds extracted from herbs and marine organisms. The results showed that emodin, a natural compound from Rheum palmatum Linn, inhibited DPP4 activity with an in vitro IC 50 of 5.76 µM without inhibiting either DPP8 or DPP9. A docking model revealed that emodin binds to DPP4 protein through Glu205 and Glu206, although with low affinity. Moreover, emodin treatment (3, 10 and 30 mg/kg, P.O.) in mice decreased plasma DPP4 activity in a dose-dependent manner. Our study suggests that emodin inhibits DPP4 activity and may represent a novel therapeutic for the treatment of type 2 diabetes.

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“…And RHL was suggested to suppress the progression of breast and ovarian cancer, hepatocellular carcinoma, cervical cancer and lung carcinoma mainly by downregulation of Bcl-2 and cyclin D expression and upregulation of BAX and Bim expression (18). In addition, RHL was demonstrated to protect the livers by reducing the expression of TNF-α and IL-6 and the phosphorylation of SREBP-1c and ERK1/2 in diabetic mice (19). In the present study, we mainly evaluated the effects of RHL on failed heart.…”

Section: Discussionmentioning

confidence: 99%

Improved heart failure by Rhein lysinate is associated with p38MAPK pathway

et al. 2018

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Abstract. The present study aimed to explore the role of Rhein lysinate (RHL) in neonatal rat ventricular myocytes (NRVMs) and congestive heart failure induced by co-arctation of the abdominal aorta. Male Sprague-Dawley rats were divided into 3 groups randomly: co-arctation of abdominal aorta group (A group, n=10), sham operation group (SH group, n=10) and RHL treatment rats (A+RHL group, n=10). To establish an in vitro oxidative stressed cardiomyocyte model, NRVMs were treated with 10 µM H 2 O 2 for 24 h. MTT assay indicated that H 2 O 2 treatment reduced primary cardiomyocyte viability in a time-and dose-dependent manner, whereas RHL abolished the detrimental effects of H 2 O 2 , indicating a protective role of RHL. Further study demonstrated that H 2 O 2 -induced reactive oxygen species (ROS) production was reversed by RHL. Then, TUNEL staining was carried out and the results revealed that H 2 O 2 markedly enhanced primary cardiomyocyte apoptosis. Conversely, RHL incubation decreased H 2 O 2 -induced cell apoptosis, indicating the protective role of RHL in primary cardiomyocytes. Furthermore, abnormal p38 activation was identified in the failed heart. Notably, treatment with RHL reduced p38 activation. In addition, RHL significantly enhanced the expression of anti-apoptotic protein, B cell lymphoma (Bcl)-2, however markedly reduced the protein level of Bcl-2 associated X, apoptosis regulator in primary cardiomyocytes, indicating its anti-apoptotic role in the cardiac setting. Overall, RHL protects heart failure primarily by reducing ROS production and cardiomyocyte apoptosis via suppressing p38 mitogen activated protein kinase activation.

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The protection of Rhein lysinate to liver in diabetic mice induced by high-fat diet and streptozotocin

Cited by 16 publications

References 24 publications

Rhein lysinate decreases inflammation and adipose infiltration in KK/HlJ diabetic mice with non-alcoholic fatty liver disease

Rhein lysinate decreases inflammation and adipose infiltration in KK/HlJ diabetic mice with non-alcoholic fatty liver disease

Screening of a natural compound library identifies emodin, a natural compound from Rheum palmatum Linn that inhibits DPP4

Improved heart failure by Rhein lysinate is associated with p38MAPK pathway

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