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    Attenuation of Kirenol InflammationInduced by Ischemic/ Reperfusion Cerebral Infarction Stroke via TLR4/ NLRP3 Signaling Pathway: An in vivo Approach

    Debo Yun1★, Yujiao Yang2★, Bin Shang1, Heng Dong1, Bo Luo1, Tahani Awad Alahmadi3, Qing Luo4★★ Corresponding author

    1. 1Department of Neurosurgery, Nanchong Central Hospital, Second Clinical Medical College of North Sichuan Medical College.
    2. 2Department of Anesthesiology, Affiliated Hospital of North Sichuan Medical College, Nanchong City, 637000, China.
    3. 3Department of Pediatrics, College of Medicine and King Khalid University Hospital, King Saud University, Medical City, Riyadh -11461, Saudi Arabia.
    4. 4Department of Ultrasound, Nanchong Central Hospital. Second Clinical Medical College of North Sichuan Medical College, Nanchong City, 637000, China.

    CORRESPONDENCE

    Debo Yun

    Department of Neurosurgery, Nanchong Central Hospital, Second Clinical Medical College of North Sichuan Medical College.

    lq469342885@sina.com

    Received: 27-07-2020; Revised: 13-08-2020; Accepted: 16-02-2021.

    Volume 17, Issue 74 · pp. 268–274 · PUBLISHED 12 July 2021 · DOI: 10.4103/pm.pm_261_20

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Objective: In this study, we examined the therapeutic role of kirenol against I/R‑induced neuronal damage by inhibiting inflammation in Sprague‑Dawley (SD) rats. Materials and Methods: I/R was induced in SD rats and subsequently were administered with 10 and 20 mg/kg of kirenol. Then, we assessed the neurological score, brain water content, and infarct size. The level of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione, and acetylcholinesterase, as well as the levels of malondialdehyde, was measured by using standard methods. The level of tumor necrosis factor (TNF)‑α; interleukin (IL)‑1 β, IL‑4, IL‑6, and IL‑10; and vascular endothelial growth factor was measured using standard kits. The targeted messenger RNA expression (NLRP3, NLRP4, TLR‐4, TNF‐α, caspase‑1, ASC, and IL‐1β) was quantified by polymerase chain reaction technique. Histopathological analysis of the brain tissue was performed. Results: According to our results, kirenol decreased the neurological deficit score, ameliorated the motor function, suppressed oxidative stress, reduced inflammation, and mediated the inhibition of TLR4/NLRP3‑mediated inflammatory pathway. Conclusion: In conclusion, these findings demonstrate the protective effects of kirenol against I/R‑induced cerebral injury. The mechanism of action is associated with the inhibition of inflammation through halting the TLR4/NLRP3 signaling pathway. In summary, kirenol is a potentially new compound which can be used to improve therapeutic strategies for stroke treatments.

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      Yun, D., Yang, Y., Shang, B., Dong, H., Luo, B., Alahmadi, T. A., & Luo, Q. (2021). Attenuation of Kirenol InflammationInduced by Ischemic/ Reperfusion Cerebral Infarction Stroke via TLR4/ NLRP3 Signaling Pathway: An in vivo Approach. Pharmacognosy Magazine, 17(74), 268–274. https://doi.org/10.4103/pm.pm_261_20