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ข้อมูลการเผยแพร่ผลงาน
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| ชื่อบทความ |
Clausena Harmandiana root extract attenuated cognitive impairments via reducing amyloid accumulation and neuroinflammation in Aβ1-42-induced rats |
| วัน/เดือน/ปี ที่ได้ตอบรับ |
11 เมษายน 2565 |
| วารสาร |
| ชื่อวารสาร |
BMC Complementary Medicine and Therapies |
| มาตรฐานของวารสาร |
SCOPUS |
| หน่วยงานเจ้าของวารสาร |
Springer Nature |
| ISBN/ISSN |
2662-7671 |
| ปีที่ |
22 |
| ฉบับที่ |
1 |
| เดือน |
April |
| ปี พ.ศ. ที่พิมพ์ |
2565 |
| หน้า |
108 |
| บทคัดย่อ |
Background
Alzheimer’s disease (AD) pathogenesis is associated with amyloid-β (Aβ)-induced neuroinflammation. In AD, the activation of microglia caused by Aβ accumulation is followed by the synthesis and release of pro-inflammatory cytokines, including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNFα), and ultimately leads to cognitive impairments. Clausena harmandiana (CH) is a medicinal plant in the Rutaceae family and has been used in folk medicine to relieve illnesses such as stomachache and headache, and as a health tonic. Interestingly, CH root extract (CHRE) has several anti-inflammatory and other pharmacological activities, but there are no studies in AD-like animal models.
Objectives
This study aims to evaluate the effects of CHRE on cognitive impairments, increased Aβ1–42 protein levels, and neuroinflammation in Aβ1–42-induced rats.
Methods
Forty-eight adult male Sprague-Dawley rats (250–300 g) were randomly divided into 6 groups (n = 8) of the sham control, V + Aβ, CB + Aβ CHRE125 + Aβ, CHRE250 + Aβ, and CHRE500 + Aβ. Sodium carboxymethylcellulose, Celebrex (10 mg/kg BW) and CHRE (125, 250, and 500 mg/kg BW) were given orally or without any treatment for 35 days. On day 21, aggregated Aβ1–42 at a concentration of 1 μg/μl were injected into both lateral ventricles (1 μl/side) of all treated rats, while sterilized normal saline were injected to untreated rats. Ten days later, the novel object recognition test was performed to assess their recognition memory. At the end of the test period, an overdose of thiopental sodium (120 mg/kg BW) and transcardial perfusion with 0.9% normal saline solution were used to euthanize all rats. Then Aβ1–42 protein levels and the expression of inflammatory markers (CD11b-positive microglia, IL-1β, and TNFα) were investigated in the cerebral cortex and hippocampus.
Results
Pretreatment with CHRE at all doses could attenuate short- and long-term impairments in recognition memory. Additionally, CHRE also inhibited the increase of Aβ1–42 protein levels and the expression of inflammatory markers in both brain regions as well as receiving Celebrex.
Conclusions
This suggests that preventive treatment of CHRE might be a potential therapy against cognitive impairments via reducing Aβ1–42 protein levels and neuroinflammation caused by Aβ1–42. |
| คำสำคัญ |
Clausena harmandiana, Alzheimer’s disease, Amyloid-β, Neuroinfammation, Recognition memory |
| ผู้เขียน |
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| การประเมินบทความ |
มีผู้ประเมินอิสระ |
| สถานภาพการเผยแพร่ |
ตีพิมพ์แล้ว |
| วารสารมีการเผยแพร่ในระดับ |
นานาชาติ |
| citation |
ไม่มี |
| เป็นส่วนหนึ่งของวิทยานิพนธ์ |
เป็น |
| แนบไฟล์ |
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| Citation |
0
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