Sains Malaysiana 53(3)(2024): 575-589

http://doi.org/10.17576/jsm-2024-5303-08

 

Proteomics Shows the Role of Paederia scandens in Ameliorating Non-alcoholic Fatty Liver Disease in a Rat Model

(Proteomik Menunjukkan Peranan Paederia scandens dalam memulihkan Penyakit Hati Berlemak Bukan Alkohol pada Model Tikus)

 

JING WANG1, TIEJIN TONG1& QIANG WU1,*

 

Agricultural College, Yibin Vocational and Technical College, Yibin 644000, China

 

Received: 6 July 2023/Accepted: 9 February 2024

 

Abstract

This study was conducted to evaluate the effect of Paederia scandens on high-fat diet­induced non-alcoholic fatty liver disease (NAFLD) in a rat model and further show the therapeutic mechanisms of Paederia scandens. Thirty rats weighing 180 ± 12 g (6 weeks old) were randomly divided into three groups: A control group (CG), a high-fat diet model group (HF), and a Paederia scandens intervention group (PS). After 45 days, the rats' serum lipid metabolism, liver injury parameters, and liver proteomics were detected. The results indicated that dietary Paederia scandens significantly reduced the levels of triglycerides, total cholesterol, glucose, and low-density lipoprotein cholesterol in the NAFLD rats compared with those in the HF group. Meanwhile, decreased levels of alanine aminotransferase and aspartate transaminase were observed in rats of the PS group. In addition, 382 differentially abundant proteins were identified between the HF and PS groups. Protein-protein interaction network analysis identified 14 keystone proteins that might play critical roles in ameliorating NAFLD. In particular, Paederia scandens treatment significantly upregulated the levels of Hadh, Hadhb, Acadl, Acox1, Acox3, Cyp3a2, and Cyp1a1, which are involved in fatty acid β‑oxidation, PPAR, and cytochrome P450 signaling pathways. Hence, the data demonstrated that Paederia scandens ameliorates hepatic lipid accumulation and impairment by enhancing fatty acid β-oxidation and activating PPAR and cytochrome P450 signaling pathways. These data provide new insights into the treatment of NAFLD and suggest the potential of Paederia scandens as an effective therapy.

 

Keywords: Non-alcoholic fatty liver disease; Paederia scandens; proteomics; rat; therapeutic mechanisms

 

Abstrak

Penyelidikan ini dijalankan untuk menilai kesan Paederia scandens terhadap penyakit hati berlemak bukan alkohol (NAFLD) akibat diet tinggi lemak pada model tikus dan seterusnya menunjukkan mekanisme terapeutik Paederia scandens. Tiga puluh ekor tikus dengan berat 180 ± 12 g (6 minggu) dibahagikan secara rawak kepada tiga kumpulan: Kumpulan kawalan (CG), kumpulan model diet tinggi lemak (HF) dan kumpulan intervensi Paederia scandens (PS). Selepas 45 hari, metabolisme lipid serum tikus, parameter kecederaan hati dan proteomik hati telah dikesan. Keputusan menunjukkan bahawa diet Paederia scandens secara signifikan mengurangkan tahap trigliserida, jumlah kolesterol, glukosa dan kolesterol lipoprotein berketumpatan rendah pada tikus NAFLD berbanding dengan kumpulan HF. Sementara itu, penurunan tahap alanine aminotransferase dan aspartate transaminase diperhatikan pada tikus kumpulan PS. Di samping itu, 382 protein yang banyak berbeza telah dikenal pasti antara kumpulan HF dan PS. Analisis rangkaian interaksi protein-protein mengenal pasti 14 protein kiston yang mungkin memainkan peranan penting dalam memperbaiki NAFLD. Khususnya, rawatan Paederia scandens dengan ketara mengimbangi tahap Hadh, Hadhb, Acadl, Acox1, Acox3, Cyp3a2 dan Cyp1a1 yang terlibat dalam pengoksidaan β asid lemak, PPAR dan laluan isyarat sitokrom P450. Oleh itu, data menunjukkan bahawa Paederia scandens memperbaiki pengumpulan dan kemerosotan lipid hepatik dengan meningkatkan pengoksidaan β asid lemak dan mengaktifkan laluan isyarat PPAR dan sitokrom P450. Data ini memberikan pandangan baharu tentang rawatan NAFLD dan mencadangkan potensi Paederia scandens sebagai terapi yang berkesan.

 

Kata kunci: Mekanisme terapeutik; penyakit hati berlemak bukan alkohol; Paederia scandens; proteomik; tikus

 

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*Corresponding author; email: wuqiangfirst@163.com

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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