Dietary capsaicin-mediated attenuation of hypertension in a rat model of renovascular hypertension

Segawa, Yukiko; Hashimoto, Hiroko; Maruyama, Saki; Shintani, Miki; Ohno, Hitomi; Nakai, Yoshinobu; Osera, Tomoko; Kurihara, Nobutaka

doi:10.1080/10641963.2019.1665676

Cited by 21 publications

(17 citation statements)

References 35 publications

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“…Interestingly, in a large Mediterranean population, regular consumption of chili pepper is associated with a lower risk of total and lower death of cardiovascular disease independent of cardiovascular risk factors or adherence to a Mediterranean diet [ 16 ]. Capsaicin, as a major component of chili pepper, is a TRPV1 agonist, can improve endothelial function by diet administration in rat model of renovascular hypertension [ 17 ]. Consequently, activation of TRPV1 is quite possible to protect noninsulin-dependent diabetes patients.…”

Section: Introductionmentioning

confidence: 99%

Capsaicin Alleviates Vascular Endothelial Dysfunction and Cardiomyopathy via TRPV1/eNOS Pathway in Diabetic Rats

Wang

Zhang

Chen

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. Endothelial dysfunction and cardiomyopathy are considered to be important vascular complications associated with diabetes. This study was designed to investigate whether capsaicin (CAP), a selective TRPV1 agonist, could prevent diabetes-induced endothelial dysfunction and cardiomyopathy. Methods. Male Sprague Dawley rats aged 8 weeks were injected intraperitoneally with streptozotocin (STZ, 50 mg/kg) to establish the diabetes model. The diabetic rats were randomly divided into the untreated diabetes group (DM, 10/group) and diabetes plus CAP treatment group (DM+CAP, 10/group); meanwhile, the nondiabetic healthy rats were used as normal controls (10/group). DM+CAP group were treated with CAP by gavage for 8 weeks. The cultured mouse vascular endothelial cells were exposed to different concentrations of glucose in the presence or absence of CAP treatment. The TRPV1 inhibitor capsazepine (CPZ) and eNOS inhibitor L-NAME were used in vivo and in vitro experiment. Results. CAP treatment significantly decreased the serum total cholesterol (TC) and total triglyceride (TG) and ameliorated the pathogenesis and fibrosis in the heart, while did not significantly improve plasma glucose level and the body weights of diabetic rats. In addition, CAP enhanced the expression of TRPV1 and eNOS in the heart and normalized the vascular permeability under diabetic state. Similarly, CAP treatment also increased nitric oxide and reduced reactive oxygen species. The same results were observed in cultured mouse vascular endothelial cells by CAP treatment. These beneficial effects of CAP were abolished by either CPZ or L-NAME. Conclusions. CAP might protect against hyperglycemia-induced endothelial dysfunction and diabetic cardiomyopathy through TRPV1/eNOS pathway.

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Section: Introductionmentioning

confidence: 99%

Capsaicin Alleviates Vascular Endothelial Dysfunction and Cardiomyopathy via TRPV1/eNOS Pathway in Diabetic Rats

Wang

Zhang

Chen

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Capsaicin (CAP), the main active ingredient of chili pepper, has multiple pharmacoactivities and therapeutic applications. These include its function as an anti-inflammatory and analgesic, an antioxidant, a controller of blood pressure, a regulator of blood lipids, and other pharmacological effects (Jolayemi and Ojewole, 2013;Vianna et al, 2018;Sańchez et al, 2019;Segawa et al, 2019). Additionally, it activates TRPV1 and initiates a complex cascade of reactions, including neuronal activation, release of proinflammatory mediators and receptor desensitization.…”

Section: Introductionmentioning

confidence: 99%

Gut Microbiota Mediates the Preventive Effects of Dietary Capsaicin Against Depression-Like Behavior Induced by Lipopolysaccharide in Mice

Xia

Guo

et al. 2021

Front. Cell. Infect. Microbiol.

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Capsaicin (CAP) is an active ingredient in chili pepper that is frequently consumed. It exerts various pharmacological activities, and also has potential effects on mental illness. However, its mechanism of antidepressant effects is still unclear. Based on the emerging perspective of the gut-brain axis, we investigated the effects of dietary CAP on gut microbes in mice with depression-like behaviors induced by lipopolysaccharide (LPS). C57BL/6J male mice (four weeks old) were given specific feed (standard laboratory chow or laboratory chow plus 0.005% CAP) for 4 months. During the last five days, LPS (0.052/0.104/0.208/0.415/0.83 mg/kg, 5-day) was injected intraperitoneally to induce depression. Behavioral indicators and serum parameters were measured, and gut microbiota were identified by sequencing analysis of the 16S gene. This study showed that dietary CAP improved depressive-like behavior (sucrose preference test, forced swimming test, tail suspension test) and levels of 5-HT and TNF-α in serum of LPS-induced mice with depression-like behaviors. In addition, CAP could recover abnormal changes in depression-related microbiota. Especially at the genus level, CAP enhanced the variations in relative abundance of certain pivotal microorganisms like Ruminococcus, Prevotella, Allobaculum, Sutterella, and Oscillospira. Correlation analysis revealed changes in microbiota composition that was closely related to depressive behavior, 5-HT and TNF-α levels. These results suggested that dietary CAP can regulate the structure and number of gut microbiota and play a major role in the prevention of depression.

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“…eNOS uncoupling reduces NO availability in renovascular hypertension. NO donors and NO-derived metabolites reduce blood pressure and organ damage in experimental renovascular hypertension (Segawa et al, 2020). Therefore, understanding the function of reduced NO in renovascular hypertension stimulates the investigation of NO donors and molecules that can be converted into NO, which are potentially important to the future treatment of CVD and CKD (Pereira et al, 2022).…”

Section: Mitochondrial Dysfunction Mechanisms In Kidney Diseasesmentioning

confidence: 99%

Renoprotective potentials of small molecule natural products targeting mitochondrial dysfunction

Rahman

Akter²,

Dorotea

et al. 2022

Front. Pharmacol.

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Kidney diseases, including acute kidney injury (AKI) and chronic kidney disease (CKD), have become critical clinical, socioeconomic, and public health concerns worldwide. The kidney requires a lot of energy, and mitochondria act as the central organelle for the proper functioning of the kidney. Mitochondrial dysfunction has been associated with the pathogenesis of AKI and CKD. Natural products and their structural analogs have been sought as an alternative therapeutic strategy despite the challenges in drug discovery. Many studies have shown that small-molecule natural products can improve renal function and ameliorate kidney disease progression. This review summarizes the nephroprotective effects of small-molecule natural products, such as berberine, betulinic acid, celastrol, curcumin, salidroside, polydatin, and resveratrol. Treatment with small-molecule natural products was shown to attenuate renal oxidative stress and mitochondrial DNA (mtDNA) damage and restore mitochondrial biogenesis and dynamics in the kidneys against various injury stimuli. Therefore, small-molecule natural products should be recognized as multi-target therapeutics and promising drugs to prevent kidney diseases, particularly those with mitochondrial dysfunction.

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Dietary capsaicin-mediated attenuation of hypertension in a rat model of renovascular hypertension

Cited by 21 publications

References 35 publications

Capsaicin Alleviates Vascular Endothelial Dysfunction and Cardiomyopathy via TRPV1/eNOS Pathway in Diabetic Rats

Capsaicin Alleviates Vascular Endothelial Dysfunction and Cardiomyopathy via TRPV1/eNOS Pathway in Diabetic Rats

Gut Microbiota Mediates the Preventive Effects of Dietary Capsaicin Against Depression-Like Behavior Induced by Lipopolysaccharide in Mice

Renoprotective potentials of small molecule natural products targeting mitochondrial dysfunction

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