Effects Of Capsaicin Research Articles

Capsaicin Protects Against Nigrostriatal Neurodegeneration Induced by Rotenone

Capsaicin, the principal pungent ingredient of hot pepper exerts neuroprotective effects. In this study, the effect of capsaicin on rotenone-induced Parkinson’s disease in mice was investigated. Mice were given subcutaneous rotenone injections (1.5 mg/kg, every other day) and at the same time treated with the vehicle, L-dopa (25 mg/kg) or capsaicin at doses of 0.5 or 1.0 mg/kg orally once a day for two weeks. Biochemical indices of oxidative stress, malondialdehyde, reduced glutathione and nitric oxide were determined in brain tissue and histopathological study of the brain was done. Behavioral tests included stair, wire hanging and wood walking tests. Results showed that rotenone treatment led to significant increases in brain malondialdehyde and nitric oxide contents parallel with marked depletion of reduced glutathione. Rotenone induced degeneration of pigmented neurons in substantia nigra and of cerebral cortex and hippocampus neurons. Rotenone impaired neuromuscular strength, motor balance and coordination. Treatment with capsaicin significantly ameliorated the neuronal degeneration caused by rotenone and improved motor function. Capsaicin alleviated the increase in lipid peroxidation (malondialdehyde) and nitric oxide and prevented the depletion of reduced glutathione in brain of rotenone-treated animals. These data indicate that capsaicin protects against rotenone-induced neuronal damage and this involves decreased level of oxidative stress. Capsaicin therefore might prevent cell death in the brain of Parkinson’s disease patients.

Differential Effect of TRPV1 Modulators on Neural and Behavioral Responses to Taste Stimuli

In our diet, we ingest a variety of compounds that are TRPV1 modulators. It is important to understand if these compounds alter neural and behavioral responses to taste stimuli representing all taste qualities. Here, we will summarize the effects of capsaicin, resiniferatoxin, cetylpyridinium chloride, ethanol, nicotine, N-geranyl cyclopropylcarboxamide, Kokumi taste peptides, pH, and temperature on neural and behavioral responses to taste stimuli in rodent models and on human taste perception. The above TRPV1 agonists produced characteristic biphasic effects on chorda tympani taste nerve responses to NaCl in the presence of amiloride, an epithelial Na+ channel blocker, at low concentrations enhancing and at high concentrations inhibiting the response. Biphasic responses were also observed with KCl, NH4Cl, and CaCl2. In the presence of multiple stimuli, the effect is additive. These responses are blocked by TRPV1 antagonists and are not observed in TRPV1 knockout mice. Some TRPV1 modulators also increase neural responses to glutamate but at concentrations much above the concentrations that enhance salt responses. These modulators also alter human salt and glutamate taste perceptions at different concentration ranges. Glutamate responses are TRPV1-independent. Sweet and bitter responses are TRPV1-independent but the off-taste of sweeteners is TRPV1-dependent. Aversive responses to acids and ethanol are absent in animals in which both the taste system and the TRPV1-trigeminal system are eliminated. Thus, TRPV1 modulators differentially alter responses to taste stimuli.

Effects of capsaicin on intestinal health under antibiotic exposure

Effects of capsaicin on intestinal health under antibiotic exposure

Metabolic pathways, pharmacokinetic, and brain neurochemicals effects of capsaicin: Comprehensively insights from in vivo studies

BackgroundCapsaicin (CAP), a prominent component of chili pepper known for its potent agonistic effects on TRPV1, has attracted significant attention for its diverse physiological effects. Nevertheless, there remains a paucity of data concerning its in vivo distribution, metabolism, pharmacodynamic properties, and influence on the metabolic profile of the brain. MethodsStable isotope tracing, in vitro enzyme incubation, microdialysis coupled with UHPLC-MS/MS techniques were employed to investigate the in vivo metabolic pathways, distribution, and pharmacokinetic properties of CAP, and the potential biases in metabolic pathways was elucidate through molecular docking. Furthermore, the effect of CAP on brain metabolic profiles was assessed using untargeted metabolomics, and spatial visualization analysis was conducted through mass spectrometry imaging. ResultsCAP was distributed predominantly in the kidneys, with lower content in the liver, heart, lungs, brain, and spleen following peripheral administration, and the absorption half-life in the body was about 20 minutes. CAP primarily underwent alkyl terminal dehydrogenation, hydroxylation, and macrocyclization metabolic pathways under the action of CYP2C9, CYP2C19 and CYP2D6, resulting in at least four metabolites. Among them, the hydroxylation products were main metabolites and the dehydrogenation product 16,17-dihydrocapsaicin could interact with the key binding sites Leu515 and Thr550 of TRPV1 like CAP. CAP quickly diffused to various brain regions and the metabolic characteristics in the striatum were relatively different from that in the blood. The distribution of CAP in the brain primarily triggered the release of neurotransmitters in areas associated with reward, cognition, and memory. Both acute and chronic exposure to CAP elevated amino acid levels in cortical regions, while producing contrasting effects on nucleotide metabolites. ConclusionThis study offers an initial in-depth analysis of the distribution patterns, metabolic pathways and pharmacodynamic properties of CAP in the body and brain. These findings established a basis for further studies on CAP's pharmacology properties and its influence on the central nervous system.

Topiramate Inhibits Capsaicin-Induced Mast Cell Degranulation and CGRP Release in Rat Dura Mater

Background/Objectives: Migraine is a disease that stands out for its high prevalence and socioeconomic costs. It involves the entire trigeminovascular system, the signaling substances, and their targets. However, the role of meningeal mast cells in migraine is still unclear. To better understand one of the components of neurogenic inflammation underlying migraine pathophysiology, we developed an in vivo rat model in which the dura mater was exposed bilaterally to investigate the influence of topiramate on capsaicin-induced mast cell degranulation and CGRP release from dura mater. Methods: On the day of the experiment, rats were anesthetized, and a craniectomy was performed on each parietal bone. Test substances were applied in situ over the dura mater using the right and left sides of the dura mater for the test and control, respectively. After exposure, the dura mater was processed for mast cell staining and counting. Using this setup, the effect of capsaicin (10−3 M) was evaluated in rats of both sexes, and subsequently the effect of in situ (10−3 M, 20 µL) and (20 mg/kg/day for 10 days) topiramate treatment on mast cell degranulation and CGRP release were evaluated. Results: In both female and male rats, there was a greater amount of degranulated mast cells in the side stimulated by capsaicin compared to the control side in both females (18 ± 3% vs. 74 ± 3%; p = 0.016) and males (28 ± 2% vs. 74 ± 3%, p = 0.016). In the group treated with topiramate for 10 days prior to the experiments, capsaicin did not induce mast cell degranulation (control 20 ± 1% vs. capsaicin 22 ± 1%, p = 0.375) in contrast to animals treated for 10 days with gavage control (control 25 ± 1% vs. capsaicin 76 ± 1%, p = 0.016). Topiramate applied in situ concomitant with capsaicin did not protect the mast cells from degranulation in response to capsaicin (38 ± 2% vs. 44 ± 1%, p = 0.016). There was a significant reduction in CGRP release from the dura mater in the group treated with topiramate for 10 days compared to the control. Conclusions: This study demonstrates a novel experimental model wherein systemic administration of topiramate is observed to modulate the impact of capsaicin on meningeal mast cell degranulation.

Effects of capsaicin on esophageal peristalsis in humans using high resolution manometry.

Capsaicin-containing red pepper sauce suspension augments esophageal contraction amplitude on conventional manometry. This study used high-resolution manometry (HRM) to investigate if capsaicin infusion modulates segmental esophageal smooth muscle peristalsis in healthy adults. Sixteen healthy volunteers (mean age 37 years, 14 male) underwent HRM for the evaluation of primary peristalsis and secondary peristalsis using slow and rapid air distensions. Both primary and secondary peristalsis were assessed following infusions of capsaicin-containing red pepper sauce and saline. Capsaicin infusion significantly increased heartburn symptoms compared to saline infusion (p < 0.001), and significantly decreased threshold volumes of secondary peristalsis during rapid air distensions (p = 0.02). The frequency of secondary peristalsis during rapid air distensions was significantly increased by capsaicin infusion (p = 0.03). Neither capsaicin infusion (p = 0.06) nor saline infusion (p = 0.27) altered threshold volume during slow air distensions. Capsaicin infusion significantly increased distal contractile integral (DCI) of primary peristalsis (p = 0.04), particularly in the proximal smooth muscle segment (p = 0.048). It enhanced secondary peristalsis during rapid air distensions (p = 0.003) but not during slow air distension (p = 0.23). Saline infusion significantly increased DCI of secondary peristalsis during rapid air distension (p = 0.01). Augmentation of distension-induced secondary peristalsis can be modulated by activation of capsaicin-sensitive afferents similar to mechanosensitive afferents. Capsaicin-induced augmentation of primary peristalsis isolates to the cholinergic-mediated proximal smooth muscle segment, which warrants study in ineffective esophageal motility to determine therapeutic potential.

Lactational performance and hematological effects of capsaicin supplementation in dairy cows: A meta-analysis

A meta-analysis was performed to investigate the effects of capsaicin (CAP) on lactational performance and blood chemistry and cell counts in dairy cattle. The database comprised 11 peer-reviewed studies published between 2011 and 2024. The overall effect of CAP, challenge (e.g., ketosis, glucose tolerance, LPS), and dose were considered explanatory variables in the analysis. Lactation performance response variables included DMI, milk yield (MY), ECM yield, feed efficiency (FE), milk components, and BW. Hematological response variables included red and white blood cell counts and blood BHB, total fatty acids, insulin, and glucose concentrations. Data were analyzed using random- and mixed-effect models in the "robumeta" package in RStudio. Milk yield was increased by 2.9% by CAP when compared with control. Capsaicin supplementation increased FE by 3.4% compared with control. Milk fat concentration and yield were also increased by CAP compared with control by 2.6% and 4.0%, respectively. Blood glucose concentrations were decreased 2.5% by CAP supplementation, whereas insulin levels were unaffected. Cows fed CAP during a challenge had higher MY and FE and tended to have lower blood glucose than their control counterparts. Overall, this analysis suggests that CAP supplementation may be directly affecting host physiology by altering glucose metabolism, but further research to define the mechanism is warranted.

Racial Specificity In The Hypotensive Effects Of Dietary Capsaicin: A Spicy Conclusion

Racial Specificity In The Hypotensive Effects Of Dietary Capsaicin: A Spicy Conclusion

Capsaicin Improves Systemic Inflammation, Atherosclerosis, and Macrophage-Derived Foam Cells by Stimulating PPAR Gamma and TRPV1 Receptors.

Capsaicin, a bioactive compound found in peppers, is recognized for its anti-inflammatory, antioxidant, and anti-lipidemic properties. This study aimed to evaluate the effects of capsaicin on atherosclerosis progression. Apolipoprotein E knockout mice and their C57BL/6 controls were utilized to assess blood lipid profile, inflammatory status, and atherosclerotic lesions. We also examined the influence of capsaicin on cholesterol influx and efflux, and the role of TRPV1 and PPARγ signaling pathways in bone marrow-derived macrophages. Capsaicin treatment reduced weight gain, visceral adiposity, blood triglycerides, and total and non-HDL cholesterol. These improvements were associated with a reduction in atherosclerotic lesions in the aorta and carotid. Capsaicin also improved hepatic oxidative and inflammatory status. Systemic inflammation was also reduced, as indicated by reduced leukocyte rolling and adhesion on the mesenteric plexus. Capsaicin decreased foam cell formation by reducing cholesterol influx through scavenger receptor A and increasing cholesterol efflux via ATP-binding cassette transporter A1, an effect primarily linked to TRPV1 activation. These findings underscore the potential of capsaicin as a promising agent for atherosclerosis prevention, highlighting its comprehensive role in modulating lipid metabolism, foam cell formation, and inflammatory responses.

Capsaicin‐mediated repair of circadian disruption‐induced Intestinal barrier damage via the gut microbiota

AbstractCircadian clock serves as a regulator of gastrointestinal health, and the disruption of circadian rhythm may trigger the dysregulation of the intestinal barrier functions. This study investigated the effectiveness of capsaicin (CAP) in mitigating intestinal barrier dysfunction induced by circadian disruption in male SPF C57BL/6J mice. Our findings indicated that CAP supplementation attenuated abnormal weight gain, alterations in serum lipid levels, and misalignment in hepatic and colonic circadian clock gene expressions in mice caused by constant darkness (CD) treatment. The restoration of the intestinal barrier integrity was also observed through the increase in mucosal thickness and goblet cell numbers. Both the diversity and the circadian rhythm of gut microbiota were improved in CAP‐treated group. Correlation analysis indicated that CAP could modulate the gut microbiota by affecting intestinal barrier function and systemic metabolism in CD‐treated mice. These results highlight the potential of CAP as a functional food component in maintaining the intestinal barrier homeostasis through regulating gut microbiota.

Capsaicin modulates TRPV1, induces β-defensin expression, and regulates NF-κB in oral senescent cells and a murine model.

Aging is associated with a decline in oral immune function, marked by reduced levels of antimicrobial peptides such as defensins. Capsaicin, a bioactive component found in chili peppers, has been theorized to modulate immune responses through specific receptor pathways. This study examined the effects of aging on oral defensin levels and the potential mitigating role of capsaicin, mediated by the immune response in oral tissues. We conducted a comparative analysis between young and aged mice, with or without capsaicin supplementation, for 3 months. The effect of capsaicin was also studied in vitro in senescence-induced human oral keratinocytes. We found that aging did not reduce defensin levels uniformly but did so in some instances. Capsaicin treatment increased defensin levels in these cases, potentially through transient receptor potential cation channel subfamily V member 1 (TRPV1)-mediated pathways in the oral cavity. Capsaicin supplementation may counteract age-related declines in oral defensin levels, enabling the maintenance of oral immune function during aging.

Effect of capsaicin on monocyte differentiation in patients with chronic obstructive pulmonary disease

Introduction. It is known that monocytes and derived macrophages play an important role in the development of chronic obstructive pulmonary disease (COPD). Previously, we found that cigarette smoke-sensitive TRPV1 channels have higher expression on monocytes and macrophages of COPD patients.Aim. To investigate the effect of chronic TRPV1 activation on the differentiation of monocytes into macrophages in vitro.Materials and methods. The study included 11 patients with COPD and 7 healthy non-smoking volunteers (control). Monocytes were obtained from peripheral blood mononuclear cells by plastic adhesion. Cells were cultured for 10 days in the presence of granulocytemacrophage colony-stimulating factor (GM-CSF) or GM-CSF and the TRPV1 agonist capsaicin. On the 11th day, the cells were stimulated with lipopolysaccharides (LPS). Expression of the genes encoding the transcription factors STAT1, STAT6, IRF3, JUN, MAF, RELA, cytokines IL1B, IL6, IL8, and three reference genes B2M, RACK1 and HPRT1 was assessed by quantitative PCR with reverse transcription.Results. Initially, macrophages of COPD patients differentiated in the presence of GM-CSF had higher expression of STAT1 (2.98-fold, p=0.03) and JUN (1.6-fold, p=0.02). LPS stimulation was accompanied by upregulation of IRF3 (4.3-fold, p=0.04), RELA (1.3-fold, p=0.05) and interleukin genes. Under the action of LPS COPD macrophages had 3.2-fold higher expression of IRF3 as compared to the control (p=0.05). Capsaicin also caused upregulation of IRF3 in cells from COPD patients, thus the expression of this factor became 3.2-fold higher than in the control group (p=0.03). Differentiation with capsaicin sensitized macrophages to LPS. Under these conditions JUN expression increased both in COPD patients (1.8-fold, p=0.01) and in the control group (2.2-fold, p=0.02) as compared with cells differentiated with GM-CSF alone.Conclusion. The obtained results indicate that in resting state macrophages from COPD patients are mostly characterized by a proinflammatory M1 polarization. LPS probably leads to an additional polarization towards M2b phenotype, when compared with the control, as indicated by an increase in the level of IRF3 transcripts. Capsaicin also promotes M2b polarization of COPD macrophages and may enhance the inflammatory response of cells to LPS.

Synergistic effect of cobalt ferrite-graphene oxide based hyperthermia and capsaicin to induce apoptosis and inhibit telomerase activity in breast cancer cells

Capsaicin is a bioactive phytochemical of red and chili peppers. It has shown therapeutic properties, including anticancer activities. In this study, the potential anti-telomerase effect of capsaicin, as well as synergic inhibitory effect of this compound in combination with cobalt ferrite-graphene oxide nanocomposites was investigated on breast cancer cell line. For this purpose, cobalt ferrite/graphene oxide (CoFe2O4/GO) nanoparticles were synthesized and characterized. Then, the effect of different concentrations of capsaicin and CoFe2O4/GO nanoparticles, and their combination on the breast adenocarcinoma cell lines (MCF-7 and MCF-10A) were analyzed using MTT assay and quantitative real-time PCR for assessing their effect on the cell viability and the expression changes in telomerase reverse transcriptase (tert), Bax and Bcl2 genes, respectively. The results showed a synergistic effect of capsaicin and CoFe2O4/GO NPs on MCF-7 cell lines that reduced the IC50 value from 0.1 and 1 mg/ml for capsaicin and CoFe2O4/GO nanoparticles, to 0.05 and 0.5 mg ml−1, respectively. Moreover, telomerase and bcl2 genes expression decreased after capsaicin and CoFe2O4/GO NPs treatment; while in contrast, bax gene expression significantly increased. Consequently, capsaicin and CoFe2O4/GO NPs treatment could induce apoptosis and inhibit the growth of breast cancer cells. In conclusion, combinational treatment with capsaicin and CoFe2O4/GO NPs could be considered as an efficient therapeutic regimen for breast cancer.

Unlocking the potential of capsaicin in oral health (Review).

Capsaicin is a bioactive compound found prominently in Capsicum annuum L. plants and takes on a pivotal role in their characteristic spiciness. Previous studies have delved into the potential analgesic effect of capsaicin in various oral conditions, such as oral neuropathic pain, trigeminal neuralgia, oral mucositis, temporomandibular joint disorders and burning mouth syndrome. Capsaicin has also demonstrated promise in inhibiting the proliferation of different oral cancer cell lines. Its antimicrobial properties have also been shown to inhibit the growth of oral pathogens associated with dental caries, periodontitis and oral candidiasis. However, to harness its benefits effectively, more studies are required to establish optimal dosages for pain relief while minimizing adverse effects. In addition, investigation of the effect of capsaicin on nonpathogenic oral bacteria and viruses is warranted. Human-based research is crucial for elucidating the biomolecular mechanisms underlying the properties of capsaicin, potentially leading to the development of more effective interventions for oral health problems.

Capsaicin Reduces Obesity by Reducing Chronic Low-Grade Inflammation.

Chronic low-grade inflammation (CLGI) is associated with obesity and is one of its pathogenetic mechanisms. Lipopolysaccharide (LPS), a component of Gram-negative bacterial cell walls, is the principal cause of CLGI. Studies have found that capsaicin significantly reduces the relative abundance of LPS-producing bacteria. In the present study, TRPV1-knockout (TRPV1-/-) C57BL/6J mice and the intestinal epithelial cell line Caco-2 (TRPV1-/-) were used as models to determine the effect of capsaicin on CLGI and elucidate the mechanism by which it mediates weight loss in vivo and in vitro. We found that the intragastric administration of capsaicin significantly blunted increases in body weight, food intake, blood lipid, and blood glucose in TRPV1-/- mice fed a high-fat diet, suggesting an anti-obesity effect of capsaicin. Capsaicin reduced LPS levels in the intestine by reducing the relative abundance of Proteobacteria such as Helicobacter, Desulfovibrio, and Sutterella. Toll-like receptor 4 (TLR4) levels decreased following decreases in LPS levels. Then, the local inflammation of the intestine was reduced by reducing the expression of tumor necrosis factor (TNF)-α and interleukin (IL)-6 mediated by TLR4. Attenuating local intestinal inflammation led to the increased expression of tight junction proteins zonula occludens 1 (ZO-1) and occludin and the restoration of the intestinal barrier function. Capsaicin increased the expression of ZO-1 and occludin at the transcriptional and translational levels, thereby increasing trans-endothelial electrical resistance and restoring intestinal barrier function. The restoration of intestinal barrier function decreases intestinal permeability, which reduces the concentration of LPS entering the circulation, and reduced endotoxemia leads to decreased serum concentrations of inflammatory cytokines such as TNF-α and IL-6, thereby attenuating CLGI. This study sheds light on the anti-obesity effect of capsaicin and its mechanism by reducing CLGI, increasing our understanding of the anti-obesity effects of capsaicin. It has been confirmed that capsaicin can stimulate the expression of intestinal transmembrane protein ZO-1 and cytoplasmic protein occludin, increase the trans-epithelial electrical resistance value, and repair intestinal barrier function.

Capsaicin: Emerging Pharmacological and Therapeutic Insights.

Capsaicin, the most prominent pungent compound of chilli peppers, has been used in traditional medicine systems for centuries; it already has a number of established clinical and industrial applications. Capsaicin is known to act through the TRPV1 receptor, which exists in various tissues; capsaicin is hepatically metabolised, having a half-life correlated with the method of application. Research on various applications of capsaicin in different formulations is still ongoing. Thus, local capsaicin applications have a pronounced anti-inflammatory effect, while systemic applications have a multitude of different effects because their increased lipophilic character ensures their augmented bioavailability. Furthermore, various teams have documented capsaicin's anti-cancer effects, proven both in vivo and in vitro designs. A notable constraint in the therapeutic effects of capsaicin is its increased toxicity, especially in sensitive tissues. Regarding the traditional applications of capsaicin, apart from all the effects recorded as medicinal effects, the application of capsaicin in acupuncture points has been demonstrated to be effective and the combination of acupuncture and capsaicin warrants further research. Finally, capsaicin has demonstrated antimicrobial effects, which can supplement its anti-inflammatory and anti-carcinogenic actions.

Acute Ongoing Nociception Delays Recovery of Consciousness from Sevoflurane Anesthesia via a Midbrain Circuit.

Although anesthesia provides favorable conditions for surgical procedures, recent studies have revealed that the brain remains active in processing noxious signals even during anesthesia. However, whether and how these responses affect the anesthesia effect remains unclear. The ventrolateral periaqueductal gray (vlPAG), a crucial hub for pain regulation, also plays an essential role in controlling general anesthesia. Hence, it was hypothesized that the vlPAG may be involved in the regulation of general anesthesia by noxious stimuli. Here, we found that acute noxious stimuli, including capsaicin-induced inflammatory pain, acetic acid-induced visceral pain, and incision-induced surgical pain, significantly delayed recovery from sevoflurane anesthesia in male mice, whereas this effect was absent in the spared nerve injury-induced chronic pain. Pretreatment with peripheral analgesics could prevent the delayed recovery induced by acute nociception. Furthermore, we found that acute noxious stimuli, induced by the injection of capsaicin under sevoflurane anesthesia, increased c-Fos expression and activity in the GABAergic neurons of the ventrolateral periaqueductal gray. Specific reactivation of capsaicin-activated vlPAGGABA neurons mimicked the effect of capsaicin and its chemogenetic inhibition prevented the delayed recovery from anesthesia induced by capsaicin. Finally, we revealed that the vlPAGGABA neurons regulated the recovery from anesthesia through the inhibition of ventral tegmental area dopaminergic neuronal activity, thus decreasing dopamine (DA) release and activation of DA D1-like receptors in the brain. These findings reveal a novel, cell- and circuit-based mechanism for regulating anesthesia recovery by nociception, and it is important to provide new insights for guiding the management of the anesthesia recovery period.

Effect of Different Administered Doses of Capsaicin and Titanium Implant Osseointegration.

Background and Objectives: This study aimed to evaluate the histological and biochemical effects of capsaicin on implant osseointegration and oxidative stress. Materials and Methods: Male Wistar albino rats weighing between 250 and 300 g were used in this study. Twenty-four rats were randomly divided into three equal groups: implant + control (n = 8), implant + capsaicin-1 (n = 8), and implant + capsaicin-2 (n = 8). Additionally, 2.5 mm diameter and 4 mm length titanium implants were surgically integrated into the corticocancellous bone parts of the femurs. In the treatment groups, rats were injected intraperitoneally with 25 mg/kg (implant + capsaicin-1) and 50 mg/kg (implant + capsaicin-2) of capsaicin. No additional applications were made in the control group. Three rats in total died during and after the experiment as a result of the analyses performed on 21 animals. Results: The highest total antioxidant status value was found in capsaicin dose 2, according to the analysis. The control group had the highest total oxidant status and oxidative stress index values, while group 2 of capsaicin had the lowest. After analysis, we found that there was no observed positive effect on osteointegration in this study (p > 0.05), although the bone implant connection was higher in the groups treated with capsaicin. Conclusions: A positive effect on osteointegration was not observed in this study. This may be due to osteoclast activation. However, it was found that it has a positive effect on oxidative stress. Osteoclast activation may be the cause of this phenomenon. Capsaicin was found to have a positive effect on oxidative stress (p < 0.05). It was also observed to have a positive effect on oxidative stress.

Inhibitory effect of thymoquinone and capsaicin on Blastocystis grown in vitro

Inhibitory effect of thymoquinone and capsaicin on Blastocystis grown in vitro

Effect of Capsaicin on 3-NP-Induced Neurotoxicity: A Pre-Clinical Study.

The study objectives are to investigate the ability of capsaicin to revert the toxic effects in glutamate and lipopolysaccharide (LPS)-induced neurotoxicity in Neuro2a (N2a) cells as well as thwarting cognitive impairments, mitochondrial deficits, and oxidative insults induced by 3-nitropropanoic acid (3-NP) in a rodent model of Huntington's disease. In-vitro study with N2a cells was performed through MTT and LDH assay and their biochemical examinations were also performed. 3-NP-administered mice (n = 6) were treated with capsaicin (5, 10, and 20mg/kg) through the per-oral (p.o.) route for 7 consecutive days. Physiological and behavioral studies were performed in drug-treated mice. After behavioral studies, biochemical parameters were performed for cytokines levels, various oxidative stress parameters, and mitochondrial enzyme complex activities with mitochondrial permeability. N2a cells treated with capsaicin demonstrated neuroprotective effects and reduced neurotoxicity. Based on experimental observation, in an in-vitro study, the effective dose of CAP was 50 µM. Moreover, a 100 µM dose of capsaicin had toxic effects on neuronal cells (N2a cells). On the other hand, the effective dose of 3-NP was 20mg/kg, (p.o.) in animals (in-vivo). All tested doses of capsaicin upturned the cognitive impairment and motor in-coordination effects induced by 3-NP. 3-NP-injected mice demonstrated substantially increased pro-inflammatory cytokine concentrations, defective mitochondrial complex activity, and augmented oxidative insult. However, capsaicin at different doses reduced oxidative damage and cytokines levels and improved mitochondrial complex activity along with mitochondrial permeability. Furthermore, capsaicin (10 and 20mg/kg) improved the TNF-α concentration. These findings suggested because of the anti-inflammatory and antioxidant effect, capsaicin can be considered a novel treatment for the management of neurodegenerative disorders by reverting the antioxidant enzyme activity, pro-inflammatory cytokines concentration, and mitochondrial functions.