scholarly journals The Natural Products Targeting on Allergic Rhinitis: From Traditional Medicine to Modern Drug Discovery

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1524
Author(s):  
Suhyun Lim ◽  
Iwah Jeong ◽  
Jonghyeok Cho ◽  
Chaewon Shin ◽  
Kwan-Il Kim ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Natural Products ◽  
Intranasal Corticosteroids ◽  
Natural Substances ◽  
Modern Drug ◽  
Tnf Α ◽  
Feasible Alternative ◽  
Nfκb Pathway ◽  
Factor Α

More than 500 million people suffer from allergic rhinitis (AR) in the world. Current treatments include oral antihistamines and intranasal corticosteroids; however, they often cause side effects and are unsuitable for long-term exposure. Natural products could work as a feasible alternative, and this study aimed to review the efficacies and mechanisms of natural substances in AR therapies by examining previous literature. Fifty-seven studies were collected and classified into plants, fungi, and minerals decoction; clinical trials were organized separately. The majority of the natural products showed their efficacies by two mechanisms: anti-inflammation regulating diverse mediators and anti-oxidation controlling the activity of nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) pathway stimulated by reactive oxygen species (ROS). The main AR factors modified by natural products included interleukin (IL)-4, IL-5, IL-13, interferon-gamma (IFN-γ), tumor necrosis factor-α (TNF-α), cyclooxygenase 2 (COX-2), and phospho-ERK1/2 (p-ERK1/2). Although further studies are required to verify their efficacies and safeties, natural products can significantly contribute to the treatment of AR.

Factors mediating the hemodynamic effects of tumor necrosis factor-α in portal hypertensive rats

1999 ◽  
Vol 276 (3) ◽  
pp. G687-G693 ◽  
Author(s):  
Javier Muñoz ◽  
Agustín Albillos ◽  
María Pérez-Páramo ◽  
Irma Rossi ◽  
Melchor Alvarez-Mon
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Portal Pressure ◽  
Systemic Resistance ◽  
Short Term ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Nitric oxide, prostacyclin, and glucagon have been implicated in promoting the hyperdynamic circulatory state of portal hypertension. Recent evidence also indicates that increased tumor necrosis factor-α (TNF-α) production is involved in the pathogenesis of this hemodynamic abnormality. This study was aimed at investigating in rats with portal vein stenosis (PVS) the effects on splanchnic hemodynamics of blocking circulating TNF-α and the factors mediating the vascular action of this cytokine in this setting. Anti-TNF-α polyclonal antibodies or placebo was injected into rats ( n = 96) before and 4 days after PVS (short-term inhibition) and at 24 h and 4, 7, 10 days after PVS (long-term inhibition). Short-term TNF-α inhibition reduced portal venous inflow and cardiac index and increased splanchnic and systemic resistance. Portal pressure was unchanged, but portal-systemic shunting was decreased. After long-term TNF-α inhibition, portal venous inflow and portal pressure were unchanged, but arterial pressure and systemic resistance rose significantly. Anti-TNF-α PVS rats exhibited lower increments of systemic resistance after N ω-nitro-l-arginine methyl ester and indomethacin administration and lower serum levels of TNF-α, nitrates-nitrites, and 6-keto-PGF1α, both over the short and the long term. Serum glucagon levels rose after long-term inhibition. In conclusion, the specific role played by TNF-α in the development of the hyperdynamic state of portal hypertension appears to be mainly mediated through an increased release of nitric oxide and prostacyclin. Maintenance of the splanchnic hyperemia after long-term TNF-α inhibition could be due to a compensatory release of glucagon.

Natural limonoids protect mice from alcohol-induced liver injury

2020 ◽  
Vol 31 (5) ◽  
Author(s):  
Abacuc Valansa ◽  
Borris Rosnay Tietcheu Galani ◽  
Pascal Dieudonne Djamen Chuisseu ◽  
Armelle Tontsa Tsamo ◽  
Vincent Brice Ayissi Owona ◽  
...  
Keyword(s):  
Liver Injury ◽  
Positive Control ◽  
Negative Control ◽  
Protective Effects ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Different Doses ◽  
Better Than

AbstractBackgroundAlcoholic liver disease (ALD) is regarded as a global health problem with limited therapeutic options. Previous studies highlighted some anticancer, antiviral, and hepatoprotective activities of limonoids, but the effects of these compounds on ALD remain unknown. The present study aimed to evaluate the effect of some natural limonoids on ethanol-induced liver injury.MethodsThirty-five albino mice (Mus musculus) were administered with 40% ethanol in the presence or absence of the different limonoids [including three havanensin-type limonoids, TS1, TS3, Rubescin D isolated from an African medicinal plant, Trichilia rubescens Oliv. (Meliaceae), and one limonin], or silymarin at 50 mg/kg for 3 days. Thereafter, the effect of the most active compound was evaluated in a chronic model of ALD. For this purpose, 24 mice with each group consisting of six mice were administered orally with 40% ethanol and limonoid at different doses (50, 75, and 100 mg/kg) for 28 days. Finally, biochemical parameters such as alanine aminotransferase (ALT), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), triglyceride (TG), and tumor necrosis factor α (TNF-α) levels were quantified in liver homogenates.ResultsAll tested limonoids significantly (p < 0.01) reduced ALT levels relative to the negative control in the acute model. However, in comparison to other limonoids, limonin at 50 and 75 mg/kg significantly reduced TG, MDA, and TNF-α levels (1.8-fold); alleviated leukocyte infiltration in liver tissue; significantly increased the activity of SOD; and decreased those of CAT better than silymarin used as a positive control at 50 mg/kg.ConclusionsThese data suggest that limonin possesses protective effects on long-term alcohol poisoning partially due to antioxidant and anti-inflammatory mechanisms.

The Impact of Tumor Necrosis Factor-α and Interleukin-1β Levels and Polymorphisms on Long-Term Stroke Outcomes

2017 ◽  
Vol 79 (1-2) ◽  
pp. 38-44 ◽  
Author(s):  
Ju-Wan Kim ◽  
Man-Seok Park ◽  
Joon-Tae Kim ◽  
Hee-Ju Kang ◽  
Kyung-Yeol  Bae ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Stroke Outcomes ◽  
Tnf Α ◽  
Poor Outcomes ◽  
Factor Α ◽  
The Impact ◽  
Necrosis Factor

Background: The accuracy of predictions regarding disability that sets in after stroke could be improved by using blood biomarker measurements. This study aimed to investigate the roles of serum tumor necrosis factor alpha (TNF-α) and interleukin (IL)-1β concentrations and polymorphisms in stroke outcomes. Methods: In total, 286 patients were evaluated at the time of admission and at 2 weeks after stroke, and 222 of these patients (78%) were followed up for 1 year to evaluate the consequences of stroke during both the acute and chronic stages. Stroke outcomes were dichotomized into good and poor using the modified Rankin Scale. Results: The association of TNF-α and IL-1β concentrations and their corresponding genotypes with stroke outcomes was investigated using multivariate logistic regression. Higher TNF-α levels were associated with poor outcomes 1 year after stroke in the presence of the –850T and –308A alleles, and IL-1β levels were associated with poor 1-year stroke outcomes in the presence of the –511T and +3953T alleles. No such associations were found at 2 weeks after stroke. Conclusions: These data provide evidence that serum TNF-α and IL-1β concentrations are related to poor long-term outcomes after stroke in the presence of particular alleles.

Usage of whey protein may cause liver damage via inflammatory and apoptotic responses

2014 ◽  
Vol 34 (7) ◽  
pp. 769-779 ◽  
Author(s):  
SG Gürgen ◽  
AT Yücel ◽  
AÇ Karakuş ◽  
D Çeçen ◽  
G Özen ◽  
...  
Keyword(s):  
Whey Protein ◽  
Protein Diet ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Short Term ◽  
Tnf Α ◽  
Serum Aspartate Aminotransferase ◽  
Group 2 ◽  
Factor Α

The purpose of this study was to investigate the long- and short-term inflammatory and apoptotic effects of whey protein on the livers of non-exercising rats. Thirty rats were divided into three groups namely (1) control group, (2) short-term whey (WS) protein diet (252 g/kg for 5 days), and (3) long-term whey (WL) protein diet (252 g/kg for 4 weeks). Interleukin 1β (IL-1β), IL-6, tumor necrosis factor α (TNF-α), and cytokeratin 18 (CK-18-M30) were assessed using enzyme-linked immunosorbent assay and immunohistochemical methods. Apoptosis was evaluated using the terminal transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) method. Hepatotoxicity was evaluated by quanitation of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Based on the biochemical levels and immunohistochemical results, the highest level of IL-1β was identified in the WL group ( p < 0.01). The IL-6 and TNF-α results were slightly lower in the WS group than in the control group and were highest in the WL group ( p < 0.01). The CK-18-M30 and TUNEL results were highest in the WS group and exhibited medium intensity in the WL group ( p < 0.01). AST results were statistically significant for all groups, while our ALT groups were particularly significant between the WL and control groups ( p < 0.01). The results showed that when whey protein is used in an uninformed manner and without exercising, adverse effects on the liver may occur by increasing the apoptotic signal in the short term and increasing inflammatory markers and hepatotoxicity in the long term.

Invasive Trichophyton Rubrum Infection Occurring with Infliximab and Long-Term Prednisone Treatment

2007 ◽  
Vol 11 (2) ◽  
pp. 84-88 ◽  
Author(s):  
Abigail L. Lowther ◽  
Ally-Khan Somani ◽  
Melissa Camouse ◽  
Frances T. Florentino ◽  
Stephen C. Somach
Keyword(s):  
Trichophyton Rubrum ◽  
Fungal Spores ◽  
Giant Cells ◽  
Invasive Disease ◽  
Term Treatment ◽  
Systemic Steroids ◽  
Tnf Α ◽  
Long Term Treatment ◽  
Factor Α

Background: A 64-year-old woman presented with erythematous plaques, tender nodules, and pustules of the dorsal right hand and both legs following long-term treatment with systemic steroids and infliximab. Skin biopsy demonstrated dermal inflammation with foci of necrosis and multinucleated giant cells containing fungal spores. Tissue culture grew Trichophyton rubrum. Objective: To report a case that demonstrates the pathophysiology of invasive T. rubrum infection, the mechanisms of action and uses of tumor necrosis factor α (TNF-α)-inhibiting drugs, and how these drugs may increase patients' risk of invasive dermatophytosis. Conclusion: Dermatophytes such as T. rubrum rarely cause invasive disease. This unusual presentation of invasive T. rubrum occurred with immunosuppression by infliximab and systemic steroids. Patients should have a thorough examination for signs of latent infection before TNF-α inhibitors are prescribed, including inspection of the skin and nails for signs of dermatophytosis.

scholarly journals Down-regulation of cyclic-nucleotide phosphodiesterase 3B in 3T3-L1 adipocytes induced by tumour necrosis factor α and cAMP

2000 ◽  
Vol 346 (2) ◽  
pp. 337-343 ◽  
Author(s):  
Tova RAHN LANDSTRÖM ◽  
Jie MEI ◽  
Marie KARLSSON ◽  
Vincent MANGANIELLO ◽  
Eva DEGERMAN
Keyword(s):  
Insulin Resistance ◽  
Tumour Necrosis Factor ◽  
Cyclic Nucleotide ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Down Regulation ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

We have used murine 3T3-L1 cells, which differentiate in culture and acquire morphological and biochemical features of mature adipocytes, as a model for studying the expression of cyclic-nucleotide phosphodiesterase (PDE) 3B activity, protein and mRNA during differentiation and during long-term treatment of the cells with tumour necrosis factor α (TNF-α), a cytokine associated with insulin resistance, and a cAMP analogue, N6,2ʹ-O-dibutyryl cAMP (dbcAMP). PDE3B activity, protein and mRNA could be detected 4 days after the initiation of differentiation of 3T3-L1 preadipocytes. Treatment of 3T3-L1 adipocytes with 10 ng/ml TNF-α for 24 h produced a maximal (50%) decrease in PDE3B activity, protein and mRNA, which was well correlated with both activation of protein kinase A (PKA) and stimulation of lipolysis, presumably reflecting an increase in intracellular cAMP concentration. To investigate the effect of cAMP on PDE3B we treated 3T3-L1 adipocytes with dbcAMP. After 4 h with 0.5 mM dbcAMP, PDE3B activity was decreased by 80%, which was also correlated with a decrease in PDE3B protein and mRNA. This effect was abolished in the presence of N-[2-(bromocinnamylamino)ethyl]-5-isoquinolinesulphonamide] (H-89), a specific PKA inhibitor. We conclude that the lipolytic effect of TNF-α involves the down-regulation of PDE3B, which is associated with increased activation of PKA, presumably owing to increased levels of cAMP. In addition, the PKA activation induced by dbcAMP resulted in the down-regulation of PDE3B. These results, which suggest that PDE3B is a novel target for long-term regulation by TNF-α and cAMP, could contribute to the understanding of the mechanisms of insulin resistance.

Acute and chronic neurological consequences of early-life Zika virus infection in mice

2018 ◽  
Vol 10 (444) ◽  
pp. eaar2749 ◽  
Author(s):  
Isis Nem de Oliveira Souza ◽  
Paula S. Frost ◽  
Julia V. França ◽  
Jéssica B. Nascimento-Viana ◽  
Rômulo L. S. Neris ◽  
...  
Keyword(s):  
Zika Virus ◽  
Zikv Infection ◽  
Behavioral Deficits ◽  
Chemically Induced ◽  
Tnf Α ◽  
Effective Therapeutic Strategy ◽  
Short And Long Term ◽  
Factor Α ◽  
Necrosis Factor

Although congenital Zika virus (ZIKV) exposure has been associated with microcephaly and other neurodevelopmental disorders, long-term consequences of perinatal infection are largely unknown. We evaluated short- and long-term neuropathological and behavioral consequences of neonatal ZIKV infection in mice. ZIKV showed brain tropism, causing postnatal-onset microcephaly and several behavioral deficits in adulthood. During the acute phase of infection, mice developed frequent seizures, which were reduced by tumor necrosis factor–α (TNF-α) inhibition. During adulthood, ZIKV replication persisted in neonatally infected mice, and the animals showed increased susceptibility to chemically induced seizures, neurodegeneration, and brain calcifications. Altogether, the results show that neonatal ZIKV infection has long-term neuropathological and behavioral complications in mice and suggest that early inhibition of TNF-α–mediated neuroinflammation might be an effective therapeutic strategy to prevent the development of chronic neurological abnormalities.

Tumor necrosis factor-α inhibits store-mediated Ca2+ entry in the human hepatocellular carcinoma cell line HepG2

2001 ◽  
Vol 280 (6) ◽  
pp. C1636-C1644 ◽  
Author(s):  
Juan A. Rosado ◽  
Ivana Rosenzweig ◽  
Susanne Harding ◽  
Stewart O. Sage
Keyword(s):  
Actin Polymerization ◽  
Carcinoma Cell ◽  
Ras Proteins ◽  
Tnf Α ◽  
Hepatocellular Carcinoma Cell Line ◽  
Human Hepatocellular Carcinoma Cell ◽  
Hepatocellular Carcinoma Cell ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) is an important component of the early signaling pathways leading to liver regeneration and proliferation, but it is also responsible for several hepatotoxic effects. We have investigated the effect of TNF-α on thapsigargin (TG)-induced store-mediated Ca2+ entry (SMCE) in the human hepatocellular carcinoma cell line HepG2. In these cells, short-term (10 min) exposure to TNF-α slightly increased SMCE. In contrast, long-term (12 h) exposure to TNF-α significantly reduced SMCE. This effect was reversed by coincubation with atrial natriuretic peptide (ANP), which itself had no effect on SMCE. Cytochalasin D and latrunculin A, inhibitors of actin polymerization, abolished SMCE. Long-term exposure of HepG2 cells to TNF-α abolished TG-induced actin polymerization and membrane association of Ras proteins. When TNF-α was added in combination with ANP, these effects were reduced. These findings suggest that in HepG2 cells, TNF-α inhibits SMCE by affecting reorganization of the actin cytoskeleton, probably by interfering with the activation of Ras proteins, and that ANP protects against these inhibitory effects of TNF-α.

Inflammatory cytokines, behaviour and age as determinants of self-rated health in women

2007 ◽  
Vol 112 (6) ◽  
pp. 363-373 ◽  
Author(s):  
Anna-Lena Undén ◽  
Anna Andréasson ◽  
Stig Elofsson ◽  
Kerstin Brismar ◽  
Linda Mathsson ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Age Groups ◽  
Subjective Health ◽  
Health And Wellbeing ◽  
Self Rated Health ◽  
Il Interleukin ◽  
Tnf Α ◽  
Factor Α ◽  
The Impact

Self-rated health is a powerful and independent predictor of long-term health, but its biological basis is unknown. We have shown previously that self-rated health is associated with increased levels of circulating cytokines in women. The main aim of the present study was to increase the understanding of the association between markers of wellbeing, such as self-rated health, and cytokines and to investigate the impact of age on these associations. In 174 female consecutive primary health care patients divided into three age groups, we examined subjective ratings of health and aspects of wellbeing and circulating levels of IL (interleukin)-1β, IL-1ra (IL-1 receptor antagonist), IL-6 and TNF-α (tumour necrosis factor-α). Poor self-rated health was significantly associated with higher levels of TNF-α in all of the age groups. For IL-1β and IL-1ra, the correlations with self-rated health were significant only in the oldest age group. Lower ratings of other measurements of health and wellbeing were related to higher levels of cytokines, most pronounced for TNF-α and IL-1β, and in the middle and olderst age groups. More symptoms resembling a sickness response induced by inflammation were implicated to be associated with lower self-rated health. The strength of the association between inflammatory cytokines and poor health perception increased with advanced age, indicating an increased vulnerability for inflammatory activity during aging. It is suggested that higher levels of TNF-α are connected to a sickness response that, in turn, is connected to self-rated health. The results provide a possible psychobiological basis to understand better diffuse subjective symptoms and poor subjective health in women.

scholarly journals Gut microbiome dysbiosis alleviates the progression of osteoarthritis in mice

2020 ◽  
Vol 134 (23) ◽  
pp. 3159-3174
Author(s):  
Zhiyuan Guan ◽  
Jialin Jia ◽  
Chenggui Zhang ◽  
Tiantong Sun ◽  
Wang Zhang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
Joint Injury ◽  
Trabecular Thickness ◽  
Tnf Α ◽  
Factor Α ◽  
The Relationship ◽  
Gut Microbiota Dysbiosis

Abstract Gut microbiota dysbiosis has been studied under the pathological conditions of osteoarthritis (OA). However, the effect of antibiotic-induced gut flora dysbiosis on OA remains incompletely understood at present. Herein, we used a mouse (8 weeks) OA model of destabilization of the medial meniscus (DMM) and gut microbiome dysbiosis induced by antibiotic treatment with ampicillin and neomycin for 8 weeks. The results show that antibiotic-induced intestinal microbiota dysbiosis reduced the serum level of lipopolysaccharide (LPS) and the inflammatory response, such as suppression of the levels of tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6), which can lead to decreased matrix metalloprotease-13 (MMP-13) expression and improvement of OA after joint injury. In addition, trabecular thickness (Tb.Th) and osteophyte scores were increased significantly in antibiotic-induced male mice compared with female mice. We further used network correlation analysis to verify the effect of gut microbiota dysbiosis on OA. Therefore, the present study contributes to our understanding of the gut–joint axis in OA and reveals the relationship between the inflammatory response, sex and gut microbiota, which may provide new strategies to prevent the symptoms and long-term sequelae of OA. Conclusion: Our data showed that gut microbiome dysbiosis alleviates the progression of OA.

Sign in / Sign up

Export Citation Format

Share Document