Inhibitory Effect of Pycnogenol® on Airway Inflammation in Ovalbumin-Induced Allergic Rhinitis

Günel, Ceren; Demirci, Buket; Eryılmaz, Adil; Yılmaz, Mustafa; Meteoğlu, İbrahim; Ömürlü, İmran Kurt; Başal, Yeşim

doi:10.5152/balkanmedj.2016.150057

Cited by 10 publications

(9 citation statements)

References 23 publications

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“…They play an important role in regulating the differentiation of T cells from the Th2 type and the IgE isotype switching in B cells [1, 30]. However, recent studies showed that the level of the Th1 cytokine, IFN-γ, was increased in AR, which could be also inhibited by steroids treatment [4, 6, 31]. Upregulation of IFN-γ levels may act as a “supporter” for Th2 cells cytokines activity in allergic response rather than playing an inhibitory role in AR [24, 31].…”

Section: Discussionmentioning

confidence: 99%

“…However, recent studies showed that the level of the Th1 cytokine, IFN-γ, was increased in AR, which could be also inhibited by steroids treatment [4, 6, 31]. Upregulation of IFN-γ levels may act as a “supporter” for Th2 cells cytokines activity in allergic response rather than playing an inhibitory role in AR [24, 31]. Here, we found that intranasal administration with miR-133b agomir markedly inhibited eosinophils and mast cells infiltration in nasal mucosa of AR mice.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-133b Ameliorates Allergic Inflammation and Symptom in Murine Model of Allergic Rhinitis by Targeting Nlrp3

Xiao¹,

Jiang²,

Hu³

et al. 2017

Cell Physiol Biochem

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Background: Emerging evidences indicate that post-transcriptional regulation by microRNAs is critical in allergic rhinitis (AR) pathogenesis. MircroRNA-133b (miR-133b) was recently suggested as a potential predictor of AR. However, the in vivo effect of miR-133b on AR is unclear. Methods: AR model was established in BALB/c mice by intraperitoneal sensitization and intranasal challenge with ovalbumin (OVA). MiR-133b agomir was then intranasally administrated to mice after OVA challenge for another 7 days. The symptom of nasal rubbing and sneezing were recorded after the last OVA challenge. Nasal mucosa tissues and serum were collected. MiR-133b expression, serum OVA-specific immunoglobulin E (IgE) concentration, proinflammatory cytokines (TNF-α, IL-4, IL-5, IL-10 and IFN-γ) levels, and Nlrp3 inflammasome activation were measured by RT-PCR, ELISA, western blotting or immunohistochemistry, respectively. Histopathologic changes were evaluated using hematoxylin and eosin and Sirius red staining. The luciferase activity and protein expression of Nlrp3 were also determined. Results: MiR-133b expression was significantly decreased in nasal mucosa of AR mice, which was restored by nasal administration with miR-133b agomir. Upregulation of miR-133b markedly reduced the concentration of OVA-specific IgE, the frequencies of nasal rubbing and sneezing, and the levels of cytokines (TNF-α, IL-4, IL-5 and IFN-γ). Levels of IL-4, IL-5, IL-10 and IFN-γ produced by cervical lymph node cells were significantly lowered in miR-133b agomir-treated mice. Moreover, miR-133b also appeared to strongly attenuate pathological alterations and eosinophils and mast cells infiltration in nasal mucosa. Notably, we demonstrated for the first time that miR-133b negatively regulated Nlrp3 expression through binding with the 3’ untranslated region of Nlrp3. Consequently, infection of miR-133b in nasal mucosa remarkably suppressed the Nlrp3 inflammasome activation, as evidenced by reduced Nlrp3, Caspase-1, ASC, IL-18 and IL-1 expressions. Conclusion: MiR-133b alleviates allergic symptom in AR mice by inhibition of Nlrp3 inflammasome-meditated inflammation. These findings provide us an insight into the potential role of miR-133b in relation to AR treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MicroRNA-133b Ameliorates Allergic Inflammation and Symptom in Murine Model of Allergic Rhinitis by Targeting Nlrp3

Xiao¹,

Jiang²,

Hu³

et al. 2017

Cell Physiol Biochem

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“…Many studies have confirmed that polyphenol-rich plant extracts can reduce TNF-␣ expression in the liver, such as Epigallocatechin gallate, tea flowers extract, and noni juice (8,30,53). Meanwhile, it also has been reported that PYC can improve TNF-␣ expression in different tissues (17,25,52). As far as we know there is not a reliable explanation to understand why TNF␣ expression is not elevated in ApoE-knockout mice fed HCD and PYC had no effect on TNF␣ expression, which might be due to differences in mouse individual expression or limitations of experimental materials and further studies are needed.…”

Section: Discussionmentioning

confidence: 96%

Pycnogenol protects against diet-induced hepatic steatosis in apolipoprotein-E-deficient mice

Wang

Cong

Wang

et al. 2018

American Journal of Physiology-Endocrinology and Metabolism

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Pycnogenol (PYC), a combination of active flavonoids derived from French maritime pine bark, is a natural antioxidant that has various pharmacological activities. Here, we investigated the beneficial effect of PYC on diet-induced hepatic steatosis. Apolipoprotein E (ApoE)-deficient male mice were administered PYC at oral doses of 30 or 100 mg·kg·day for 2 wk in advance and were then fed a high-cholesterol and -fat diet (HCD) for 8 wk. Biochemical, immunohistochemical, and gene expression analyses were conducted to explore the effect of PYC on lipid metabolism in ApoE-deficient mice on a HCD. Short-term treatment with HCD in ApoE-deficient mice induced hepatic injuries, such as lipid metabolism disorder and hepatic histopathological changes. We found that PYC reduced body weight and the increase of serum lipids that had been caused by HCD. Supplementation of PYC significantly reduced lipid deposition in the liver, as shown by the lowered hepatic lipid content and histopathological lesions. We subsequently detected genes related to lipid metabolism and inflammatory cytokines. The study showed that PYC markedly suppressed the expression of genes related to hepatic lipogenesis, fatty acid uptake, and lipid storage while increasing the lipolytic gene, which thus reduced hepatic lipid content. Furthermore, PYC mainly reduced the expression of inflammatory cytokines and the infiltration of inflammatory cells, which were resistant to the development of hepatic steatosis. These results demonstrate that PYC protects against the occurrence and development of hepatic steatosis and may provide a new prophylactic approach for nonalcoholic fatty liver disease (NAFLD).

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“…There are countless experimental studies about pycnogenol. In this literature, the antioxidative effects of pycnogenol have been investigated in various organs and tissues, such as the eye, brain, optic nerve, nasal mucosa, peritoneum, lymph nodes, bones, heart, aorta, kidney, liver and colon in animal models [8,[10][11][12][13][19][20][21][22][23][24]. This literature information suggests that antioxidant drugs might be beneficial in preventing CP-related uterine and ovarian toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that pycnogenol is a hepatoprotective molecule which has potential anti-inflammatory properties in some chronic diseases [8,9]. Pycnogenol also inhibits histamine and proinflammatory cytokines and reduces allergic responses [10]. Icel et al reported that pycnogenol treatment was highly effective in preventing cisplatin-induced oxidative stress in ocular and optic nerve tissues [11].…”

Section: Introductionmentioning

confidence: 99%

Can pycnogenol prevent cisplatin-induced damage in uterus and ovaries?

et al. 2019

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Introduction: Cisplatin is an antineoplastic agent, which is thought to act on tissues with increased levels of reactive oxygen species and decreased levels of antioxidants. Pycnogenol is a potent antioxidant that is used in medical conditions caused by oxidative stress. The aim of our study is to demonstrate the effects of pycnogenol on cisplatin-induced uterine and ovarian damage in rats. Material and methods: Wistar albino female rats were randomly divided into 3 groups before the experiment as follows: a 2.5 mg/kg cisplatin group (CG; n = 10), a 40 mg/kg pycnogenol + 2.5 mg/kg cisplatin group (PCG; n = 10), and a healthy control group (HG; n = 10). Then, the ovaries and uteri of the rats were examined to determine malondialdehyde (MDA), total glutathione (tGSH) and superoxide dismutase (SOD) biochemical levels and the histopathological findings. Results: Our study demonstrated that, in uterine and ovarian tissues of rats administered with cisplatin, there was a decrease in the levels of tGSH and SOD, while MDA was increased; however, it was observed that these ratios were reversed in the PCG group (p < 0.05). The number of follicles in the ovarian tissues was examined in all 3 groups. When the CG group was compared with the other two groups, the number of primordial, developing and atretic follicles was low, but there was no difference in the corpus luteum count. Conclusions: Pycnogenol pretreatment alleviates cisplatin-induced uterine and ovarian injury in rats because of its antioxidative effect.

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Inhibitory Effect of Pycnogenol® on Airway Inflammation in Ovalbumin-Induced Allergic Rhinitis

Cited by 10 publications

References 23 publications

MicroRNA-133b Ameliorates Allergic Inflammation and Symptom in Murine Model of Allergic Rhinitis by Targeting Nlrp3

MicroRNA-133b Ameliorates Allergic Inflammation and Symptom in Murine Model of Allergic Rhinitis by Targeting Nlrp3

Pycnogenol protects against diet-induced hepatic steatosis in apolipoprotein-E-deficient mice

Can pycnogenol prevent cisplatin-induced damage in uterus and ovaries?

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