Modulation of T-helper cytokines and inflammatory mediators by Atropa accuminata. Royle in adjuvant induced arthritic tissues

Nisar, Albeena; Akhter, Nayeema; Singh, Gurudarshan; Akbar, Muhammad; Malik, Akhtar H.; Banday, Basharat; Zargar, Mohammad Afzal

doi:10.1016/j.jep.2014.08.008

Cited by 16 publications

(10 citation statements)

References 48 publications

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“…Interestingly, FCA also produces articular hypoemia, which nicely models the hypoxic environment found in rheumatoid arthritic joints . It has been shown in previous studies that FCA injection elicits the production and release of various inflammatory mediators such as PGE2, nitric oxide, leukotriene B2, TNF‐ α , IL‐2, and IL‐17 . These pro‐inflammatory mediators cause synovitis, polyarticular inflammation, bone resorption, periosteal bone, and proliferation and can result in joint degeneration .…”

Section: Models Of Joint Painmentioning

confidence: 73%

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Preclinical Assessment of Inflammatory Pain

2015

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While acute inflammation is a natural physiological response to tissue injury or infection, chronic inflammation is maladaptive and engenders a considerable amount of adverse pain. The chemical mediators responsible for tissue inflammation act on nociceptive nerve endings to lower neuronal excitation threshold and sensitize afferent firing rate leading to the development of allodynia and hyperalgesia, respectively. Animal models have aided in our understanding of the pathophysiological mechanisms responsible for the generation of chronic inflammatory pain and allowed us to identify and validate numerous analgesic drug candidates. Here we review some of the commonly used models of skin, joint, and gut inflammatory pain along with their relative benefits and limitations. In addition, we describe and discuss several behavioral and electrophysiological approaches used to assess the inflammatory pain in these preclinical models. Despite significant advances having been made in this area, a gap still exists between fundamental research and the implementation of these findings into a clinical setting. As such we need to characterize inherent pathophysiological pathways and develop new endpoints in these animal models to improve their predictive value of human inflammatory diseases in order to design safer and more effective analgesics.

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Section: Models Of Joint Painmentioning

confidence: 73%

“…Rat [86,88,89,93] Mice [80,91,92] onto the ears of mice produces skin inflammation, which is mainly characterized by vasodilatation, increased plasma extravasation, and edema. These changes are blocked by treatment with an NK1 antagonist [41].…”

Section: Mustard Oil-induced Painmentioning

confidence: 99%

Preclinical Assessment of Inflammatory Pain

2015

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“…Therefore, maintaining Th17/ Treg balance is important for the treatment of focal cerebral ischemia/reperfusion injury. Studies have shown that IL-17 can promote the secretion of IL-6, TNF-α and other pro-inflammatory factors, by antigen-presenting cells, and participate in and expand the host inflammatory response [13][14][15]. IL-6 is a key cytokine that can determine the differentiation of naive T cells into Th17 or Treg cells.…”

Section: Introductionmentioning

confidence: 99%

Salidroside regulates imbalance of Th17/Treg and promotes ischemic tolerance by targeting STAT-3 in cerebral ischemia-reperfusion injury

et al. 2021

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IntroductionThe balance between Th17 and Treg cells controls the immune response and is an important regulator of helper T cells acting on autoimmune diseases. Focal cerebral ischemia-reperfusion injury can induce imbalance of Th17/Treg cells in the brain and the peripheral immune system of rats. The aim of this study was to investigate the effect of salidroside (Sal) on the ratio of Th17 and Treg cells in an adult rat model of middle cerebral artery occlusion (MCAO).Material and methodsForty rats were divided into 4 groups: normal group, sham group, surgery group, and Sal group. After treatment, the neurological deficits in rats were evaluated. Peripheral blood mononuclear cells were isolated and the count of Th17 and Treg cells was detected by flow cytometry. The infarct size and expression of RORt and Foxp3 were detected in rat brain tissue. Rat spleen cells were isolated, CD4+ T cells were purified by immunomagnetic beads. Treg cells were induced by adding cytokine TGF-. Th17 cells were induced by adding cytokine IL-6. The expression of STAT-3 was inhibited by SiRNA, and the effect of Sal on the differentiation of Th17/Treg cells was analyzed. The expression levels of IL-6, TNF-, MCP-1, STAT-3 and NF--B2 proteins were examined.ResultsThe results show that MCAO can induce an imbalance of Th17 and Treg cells in peripheral blood of rats. Sal treatment can significantly reduce the neurological deficit and infarct size of MCAO rats, reverse the oxidative stress of rat brain tissue, and inhibit the apoptosis of brain cells in MCAO rats. In the brain tissue of MCAO rats, Sal could significantly inhibit the expression of IL-6, TNF-, MCP-1, STAT-3 and NF--B2. Down-regulation of STAT-3 significantly reversed the therapeutic effects of Sal treatment.ConclusionsOur results indicate that Sal can increase the tolerance of rat brain tissue to ischemia, inhibit cell apoptosis and reduce oxidative stress by targeting STAT-3.

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“…It has been reported that Th17 cells cause the chronic pathogenesis of rheumatoid arthritis (Gaffen, ; Fouser et al , ). Indeed, at the early stages of arthritis, the Th17 cells stimulate generation of matrix metalloproteinase and proinflammtory cytokines (Nisar et al , ). In addition, inhibiting the cytokines produced by Th17 especially IL‐17A may contribute to reduction of HIV infection (Kapewangolo et al , ).…”

Section: Introductionmentioning

confidence: 99%

“…Maximal decrease was seen at the highest dose (500 mg/kg b.w). This extract results in up‐regulation of Th2 cytokines (IL‐4 and IL‐10), and the suppression of Th1–Th17 cytokines (IL‐2, TNF‐α, IFN‐γ, IL‐12, IL‐17, IL‐6) and pro‐inflammatory mediators (PGE2, NO, IL‐1 β and LTB4) is dose dependent (Nisar et al , ).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Th1 and Th17 Cells by Medicinal Plants and Their Derivatives: A Systematic Review

et al. 2017

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Searching for new natural drugs that are capable of targeting Th1 and Th17 may lead to development of more effective treatments for inflammatory and autoimmune diseases. Most of the natural drugs can be derived from plants that are used in traditional medicine and folk medicine. The aim of this systematic review is to identify and introduce plants or plant derivatives that are effective on inflammatory diseases by inhibiting Th1 and Th17 responses. To achieve this purpose, the search terms herb, herbal medicine, herbal drug, medicinal plant, phytochemical, traditional Chinese medicine, Ayurvedic medicine, natural compound, inflammation, inflammatory diseases, Th1, Th17, T helper 1 or T helper 17 were used separately in Title/Keywords/Abstract in Web of Science and PubMed databases. In articles investigating the effect of the medicinal plants and their derivatives in inhibiting Th1 and Th17 cells, the effects of eight extracts of the medicinal plants, 21 plant-based compounds and some of their derivatives, and eight drugs derived from the medicinal plants' compounds in inhibiting Th1 and Th17 cells were reviewed. The results showed that medicinal plants and their derivates are able to suppress Th17 and Th1 T cell functions as well as cytokine secretion and differentiation. The results can be used to produce herbal drugs that suppress Th, especially Th17, responses. Copyright © 2017 John Wiley & Sons, Ltd.

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Modulation of T-helper cytokines and inflammatory mediators by Atropa accuminata. Royle in adjuvant induced arthritic tissues

Cited by 16 publications

References 48 publications

Preclinical Assessment of Inflammatory Pain

Preclinical Assessment of Inflammatory Pain

Salidroside regulates imbalance of Th17/Treg and promotes ischemic tolerance by targeting STAT-3 in cerebral ischemia-reperfusion injury

Inhibition of Th1 and Th17 Cells by Medicinal Plants and Their Derivatives: A Systematic Review

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