Dioscin protects against coronary heart disease by reducing oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways

Yang, Bo; Xu, Bin; Zhao, Hua; Wang, Ya‐Bin; Zhang, Jian; Li, Chuanwei; Wu, Qing; Cao, Yu‐Kang; Yang, Li; Cao, Feng

doi:10.3892/mmr.2018.9024

Cited by 49 publications

(46 citation statements)

References 37 publications

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“…We conclude from this study that the neuroprotective effects of diosgenin are mainly exerted through a reduction in the oxidative stress response and the enhancement of the oxidative defence system. The results confirmed previous findings regarding the therapeutic effects of diosgenin [39,40]. Histological analysis showed that the biochemical changes in STZ-induced diabetic mice included degeneration of sciatic nerve fibres and endometrial edema.…”

Section: Discussionsupporting

confidence: 90%

Neuroprotective effect of diosgenin in a mouse model of diabetic peripheral neuropathy involves the Nrf2/HO-1 pathway

Jin-hong

Tian

et al. 2020

BMC Complement Med Ther

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Background: Diabetic peripheral neuropathy (DPN) is one of the most common chronic complications of diabetes. Diosgenin is a natural steroidal saponin with a variety of beneficial effects, including antidiabetic effects, and is a raw material for the synthesis of carrier hormones. In our study, we aimed to assess the antioxidant effects of diosgenin in diabetic mice. Methods: Male C57 mice were fed a high-fat diet for 8 weeks and intraperitoneally injected with streptozotocin (STZ) at a dose of 100 mg/kg for 2 consecutive days. Eligible mice were divided into the normal control group (CON), diabetic group (DM), low-dose diosgenin (50 mg/kg) group (DIO50) and high-dose diosgenin (100 mg/kg) group (DIO100). Treatment was started 6 weeks after the induction of diabetes by STZ and continued for 8 weeks. Blood sugar and body weight were monitored dynamically. The behavioural effects of diosgenin were detected by a hot tail immersion test and paw tactile responses. HE staining was used to evaluate edema and degeneration of the sciatic nerve. The levels of SOD, MDA and GPx were tested according to the instructions of the respective kits. The levels of Nrf2, HO-1 and NQO1 were detected by immunofluorescence and Western blotting. Statistical analysis was performed using SPSS, and P < 0.05 was considered statistically significant. Results: Diosgenin decreased the blood glucose levels and increased the body weight of diabetic mice. There was a significant increase in the tail withdrawal latency of diabetic animals, and mechanical hyperalgesia was significantly alleviated after diosgenin treatment. Histopathological micrographs of HE-stained sciatic nerves showed improvement after diosgenin treatment. Diosgenin attenuated the level of MDA but increased the activities of SOD and GPx. Diosgenin increased the expression of Nrf2, HO-1 and NQO1. Conclusions: Our results demonstrate that diosgenin can ameliorate behavioural and morphological changes in DPN by reducing oxidative stress. The Nrf2/HO-1 signalling pathway was involved in its neuroprotective effects.

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Section: Discussionsupporting

confidence: 90%

Neuroprotective effect of diosgenin in a mouse model of diabetic peripheral neuropathy involves the Nrf2/HO-1 pathway

Jin-hong

Tian

et al. 2020

BMC Complement Med Ther

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“…Tai Chi belongs to a kind of aerobic exercise and should have similar function in regulating fat metabolism. MAPK pathway plays an important role in the pathogenesis of CHD [31] and is regulated by miR-126 [34]. e present findings demonstrated that Tai Chi intervention reduced the relative levels of miR-126 ( Figure 1) and the levels of MAPK signaling (Figures 2 and 3).…”

Section: Discussionsupporting

confidence: 55%

“…However, the related molecular mechanism of Tai Chi exercise remains unclear. Mitogen-activated protein kinase (MAPK) signaling plays a critical role in the pathogenesis of CHD [31,32] and can be activated by miR-126 [33,34]. miR-126 is an independent risk factor of CHD and affects many important gene expression [35,36].…”

Section: Introductionmentioning

confidence: 99%

Tai Chi Improves Coronary Heart Disease Risk by Inactivating MAPK/ERK Pathway through Serum miR‐126

Zhang

Wang

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Background. Tai Chi is effective in preventing heart disease (CHD) risk, but the molecular mechanism remains unclear. Mitogen-activated protein kinase (MAPK) signaling plays a critical role in the pathogenesis of CHD and can be activated by miR-126. Tai Chi may exert its protective function through the miR-126-modulated MAPK pathway. Methods. The CHD patients after PCI were randomized into the CG group (CG) (n = 19, normal care) and Tai Chi group (TG) (Tai Chi intervention, n = 17). Epicardial adipose tissue volume (EATV) (one main adverse cardiovascular event of CHD), HR (heart rate), QoL (quality of life) scores, and balance performance were measured in the two groups. The body fat content, abdominal subcutaneous fat, and visceral fat were measured to reflect the improvement of adipose tissue dysfunction. The levels of miR-126 and MAPK-associated molecules were measured in peripheral blood leukocytes. Meanwhile, the effects of miR-126 silence and mimic on MAPK-associated molecules were also explored in cardiac cell H9C2. Results. After the 3-month intervention, Tai Chi reduced EATV and HR and increased QoL scores and balance performance, respectively (P<0.05). The fat percentage, body fat mass, and BMI were also significantly reduced after Tai Chi intervention (P<0.05). The levels of miR-126, MAPK, JNK, and ERK in the TG group were lower than those in the CG group (P<0.05). The miR-126 levels had a strong relationship with the values of EATV, HR, and QoL scores (P<0.05). miR-126 silence or mimic inactivated or activated MAPK-associated molecules in the cardiac cell lines. Conclusions. Tai Chi improved CHD risk by inactivating the MAPK/ERK pathway via serum miR-126.

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“…Importantly, many effects of SIRT1 that are relevant to the suppression or avoidance of inflammation have been also observed upon treatment with melatonin (Figure ). In addition to the inhibition of NF‐κB activation, to Nrf2 upregulation, and to the avoidance of NLRP3 inflammasome activation, several further anti‐inflammatory actions of SIRT1 have become known. This concerns, for example, an inhibition of TLR4, which was demonstrated in renal collecting duct cells by either SIRT1 overexpression or activation by SRT1720, effects that were blocked by Sirt1 siRNA or the sirtuin inhibitors sirtinol and EX527 .…”

Section: Downstream Factors Of Melatonin's Actions With Relevance To mentioning

confidence: 99%

Melatonin and inflammation—Story of a double‐edged blade

Hardeland

2018

Journal of Pineal Research

360

350

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Melatonin is an immune modulator that displays both pro‐ and anti‐inflammatory properties. Proinflammatory actions, which are well documented by many studies in isolated cells or leukocyte‐derived cell lines, can be assumed to enhance the resistance against pathogens. However, they can be detrimental in autoimmune diseases. Anti‐inflammatory actions are of particular medicinal interest, because they are observed in high‐grade inflammation such as sepsis, ischemia/reperfusion, and brain injury, and also in low‐grade inflammation during aging and in neurodegenerative diseases. The mechanisms contributing to anti‐inflammatory effects are manifold and comprise various pathways of secondary signaling. These include numerous antioxidant effects, downregulation of inducible and inhibition of neuronal NO synthases, downregulation of cyclooxygenase‐2, inhibition of high‐mobility group box‐1 signaling and toll‐like receptor‐4 activation, prevention of inflammasome NLRP3 activation, inhibition of NF‐κB activation and upregulation of nuclear factor erythroid 2‐related factor 2 (Nrf2). These effects are also reflected by downregulation of proinflammatory and upregulation of anti‐inflammatory cytokines. Proinflammatory actions of amyloid‐β peptides are reduced by enhancing α‐secretase and inhibition of β‐ and γ‐secretases. A particular role in melatonin's actions seems to be associated with the upregulation of sirtuin‐1 (SIRT1), which shares various effects known from melatonin and additionally interferes with the signaling by the mechanistic target of rapamycin (mTOR) and Notch, and reduces the expression of the proinflammatory lncRNA‐CCL2. The conclusion on a partial mediation by SIRT1 is supported by repeatedly observed inhibitions of melatonin effects by sirtuin inhibitors or knockdown.

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Dioscin protects against coronary heart disease by reducing oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways

Cited by 49 publications

References 37 publications

Neuroprotective effect of diosgenin in a mouse model of diabetic peripheral neuropathy involves the Nrf2/HO-1 pathway

Neuroprotective effect of diosgenin in a mouse model of diabetic peripheral neuropathy involves the Nrf2/HO-1 pathway

Tai Chi Improves Coronary Heart Disease Risk by Inactivating MAPK/ERK Pathway through Serum miR‐126

Melatonin and inflammation—Story of a double‐edged blade

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