Tetrahydrocurcumin in combination with deferiprone attenuates hypertension, vascular dysfunction, baroreflex dysfunction, and oxidative stress in iron-overloaded mice

Sangartit, Weerapon; Pakdeechote, Poungrat; Kukongviriyapan, Veerapol; Donpunha, Wanida; Shibahara, Shigeki; Kukongviriyapan, Upa

doi:10.1016/j.vph.2016.10.001

Cited by 33 publications

(20 citation statements)

References 54 publications

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“…All those evidences suggest that targeting SIRT1 may be a promising treatment strategy for DCM. THC, the major active metabolite of natural product curcumin, possesses a variety of pharmacological activities similar to curcumin, such as antioxidative, anti-inflammatory, anticancer, antidiabetic, and neuroprotective properties [13, 14, 37–40]. Moreover, THC was found to be more stable and shows a higher bioavailability than curcumin, which were generally considered as main limitations for the clinical application of curcumin [37, 41–43].…”

Section: Discussionmentioning

confidence: 99%

Tetrahydrocurcumin Ameliorates Diabetic Cardiomyopathy by Attenuating High Glucose-Induced Oxidative Stress and Fibrosis via Activating the SIRT1 Pathway

Zhai

Jiang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Hyperglycemia-induced oxidative stress and fibrosis play a crucial role in the development of diabetic cardiomyopathy (DCM). Tetrahydrocurcumin (THC), a major bioactive metabolite of natural antioxidant curcumin, is reported to exert even more effective antioxidative and superior antifibrotic properties as well as anti-inflammatory and antidiabetic abilities. This study was designed to investigate the potential protective effects of THC on experimental DCM and its underlying mechanisms, pointing to the role of high glucose-induced oxidative stress and interrelated fibrosis. In STZ-induced diabetic mice, oral administration of THC (120 mg/kg/d) for 12 weeks significantly improved the cardiac function and ameliorated myocardial fibrosis and cardiac hypertrophy, accompanied by reduced reactive oxygen species (ROS) generation. Mechanically, THC administration remarkably increased the expression of the SIRT1 signaling pathway both in vitro and in vivo, further evidenced by decreased downstream molecule Ac-SOD2 and enhanced deacetylated production SOD2, which finally strengthened antioxidative stress capacity proven by repaired activities of SOD and GSH-Px and reduced MDA production. Additionally, THC treatment accomplished its antifibrotic effect by depressing the ROS-induced TGFβ1/Smad3 signaling pathway followed by reduced expression of cardiac fibrotic markers α-SMA, collagen I, and collagen III. Collectively, these finds demonstrated the therapeutic potential of THC treatment to alleviate DCM mainly by attenuating hyperglycemia-induced oxidative stress and fibrosis via activating the SIRT1 pathway.

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Section: Discussionmentioning

confidence: 99%

Tetrahydrocurcumin Ameliorates Diabetic Cardiomyopathy by Attenuating High Glucose-Induced Oxidative Stress and Fibrosis via Activating the SIRT1 Pathway

Zhai

Jiang

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…Similarly, another study demonstrated that tetrahydrocurcumin and octahydrocurcumin have anti-inflammatory activity, as they inhibited the expression of COX-2 and suppressed the nuclear factor-kB pathway [92]. In addition, tetrahydrocurcumin was used as an antioxidant to alleviate hypertension and vascular dysfunction in iron-overloaded mice [93]. Figure 4: Curcumin metabolism through oral and other routes of administration [83].…”

Section: Metabolism Of Curcuminmentioning

confidence: 99%

Improvement of Curcumin Bioavailability for Medical Applications

Her¹,

Venier-Julienne²,

Roger³

2018

Med Aromat Plants

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“…Moreover, the ability of THC to stimulate the activities of other antioxidant enzymes further strengthens its antioxidative characteristics [19, 20]. However, the inner mechanism through which THC protects the brain from oxidative insult is not clear.…”

Section: Discussionmentioning

confidence: 99%

Tetrahydrocurcumin Provides Neuroprotection in Experimental Traumatic Brain Injury and the Nrf2 Signaling Pathway as a Potential Mechanism

Guan

Chen

Lin

et al. 2017

Neuroimmunomodulation

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The protective effect of tetrahydrocurcumin (THC) after experimental traumatic brain injury (TBI) has been demonstrated, as demonstrated by the inhibition of oxidative stress, mitochondrial dysfunction, and apoptosis. However, the mechanisms underlying this effect are still not well understood. This study was to investigate the neuroprotective effects of THC, and its potential mechanisms, in a rat model of TBI. To this end, rats were divided into 4 groups: the sham group, the TBI group, the TBI + vehicle (V) group, and the TBI + THC group. THC or V was administered via intraperitoneal injection to rats in the TBI + V and TBI + THC groups 30 min after TBI. After euthanasia (24 h after TBI), neurological scores, brain water content, and neuronal cell death in the cerebral cortex were recorded. Brain samples were collected after neurological scoring for further analysis. THC treatment alleviated brain edema, attenuated TBI-induced neuronal cell apoptosis, and improved neurobehavioral function. In addition, NFE2-related factor 2 (Nrf2) expression was upregulated following TBI. These results suggest that THC improves neurological outcome after TBI, possibly by activating the Nrf2 signaling pathway.

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Tetrahydrocurcumin in combination with deferiprone attenuates hypertension, vascular dysfunction, baroreflex dysfunction, and oxidative stress in iron-overloaded mice

Cited by 33 publications

References 54 publications

Tetrahydrocurcumin Ameliorates Diabetic Cardiomyopathy by Attenuating High Glucose-Induced Oxidative Stress and Fibrosis via Activating the SIRT1 Pathway

Tetrahydrocurcumin Ameliorates Diabetic Cardiomyopathy by Attenuating High Glucose-Induced Oxidative Stress and Fibrosis via Activating the SIRT1 Pathway

Improvement of Curcumin Bioavailability for Medical Applications

Tetrahydrocurcumin Provides Neuroprotection in Experimental Traumatic Brain Injury and the Nrf2 Signaling Pathway as a Potential Mechanism

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