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Potensi Antidiabetes Ekstrak Etanolik Daun Dendrocalamus asper melalui Inhibisi Enzim Alfa Amilase secara In Vitro dan In Silico

Rahma Nur Ismadi, Dr. Tri Rini Nuringtyas, S.Si., M.Sc.

2026 | Skripsi | BIOLOGI

Diabetes melitus merupakan penyakit metabolik yang ditandai oleh hiperglikemia kronis dan dapat dikendalikan melalui penghambatan enzim pencerna karbohidrat, salah satunya alfa amilase. Penelitian ini bertujuan untuk menganalisis potensi antidiabetes ekstrak etanol dan fraksi daun Dendrocalamus asper berdasarkan aktivitas inhibisi alfa-amilase secara in vitro, mengidentifikasi dugaan senyawa metabolit sekunder menggunakan LC-HRMS, serta menganalisis potensi senyawa kandidat sebagai inhibitor alfa-amilase secara in silico melalui molecular docking. Ekstraksi daun D. asper dilakukan menggunakan etanol 70%, dilanjutkan dengan fraksinasi cair-cair menggunakan n-heksan, etil asetat, dan etanol-akuades. Aktivitas inhibisi alfa amilase diuji menggunakan metode DNS, sedangkan identifikasi senyawa dilakukan dengan LC-HRMS. Senyawa kandidat kemudian diseleksi berdasarkan parameter drug-likeness, absorpsi gastrointestinal, toksisitas, dan prediksi aktivitas biologis sebelum dilakukan molecular docking terhadap reseptor alfa amilase 2QV4. Hasil penelitian menunjukkan bahwa rendemen ekstrak etanol sebesar 6,86%, sedangkan rendemen fraksi n-heksan, etil asetat, dan etanol-akuades berturut-turut sebesar 10,00%, 5,00%, dan 47,00%. Ekstrak etanol memiliki aktivitas inhibisi tertinggi dengan nilai IC50 sebesar 1213,91 ± 82,37 mg/L, sedangkan seluruh fraksi belum mencapai inhibisi 50% hingga konsentrasi 1600 mg/L. Analisis LC-HRMS menghasilkan 55 dugaan senyawa yang didominasi oleh flavonoid dan turunannya. Hasil molecular docking menunjukkan bahwa Apigenin memiliki nilai binding affinity terbaik di antara senyawa uji, yaitu -8,9 kcal/mol, tetapi afinitasnya belum sebaik acarbose sebagai ligan pembanding. Berdasarkan hasil tersebut, ekstrak daun D. asper menunjukkan aktivitas inhibisi alfa amilase, namun kurang potensial sebagai kandidat antidiabetes melalui mekanisme ini dibandingkan acarbose. 

Diabetes mellitus is a metabolic disease characterized by chronic hyperglycemia and can be managed through the inhibition of carbohydrate-digesting enzymes, including alpha amylase. This study aimed to analyze the antidiabetic potential of ethanol extract and fractions of Dendrocalamus asper leaves based on in vitro alpha amylase inhibitory activity, identify putative secondary metabolites using LC-HRMS, and evaluate candidate compounds as alpha amylase inhibitors through in silico molecular docking. The leaves of D. asper were extracted using 70% ethanol and fractionated using n-hexane, ethyl acetate, and ethanol-aqueous solvents. The alpha amylase inhibitory activity was evaluated using the DNS method, while compound identification was performed using LC-HRMS. Candidate compounds were selected based on drug-likeness, gastrointestinal absorption, toxicity, and biological activity prediction before molecular docking against the alpha amylase receptor 2QV4. The results showed that the ethanol extract yield was 6.86%, while the yields of n-hexane, ethyl acetate, and ethanol fractions were 10.00%, 5.00%, and 47.00%, respectively. The ethanol extract exhibited the highest inhibitory activity with an IC50 value of 1213.91 ± 82.37 mg/L, whereas all fractions did not reach 50% inhibition at the highest tested concentration of 1600 mg/L. LC-HRMS analysis identified 55 putative compounds, predominantly flavonoids and their derivatives. Molecular docking results showed that Apigenin had the best binding affinity among the tested compounds, with a value of -8.9 kcal/mol; however, its affinity was less favorable than acarbose as the reference ligand. These findings indicate that D. asper leaves exhibit alpha amylase inhibitory activity but have limited potential as antidiabetic candidates through this mechanism compared to acarbose.

Kata Kunci : diabetes melitus, Dendrocalamus asper, alfa amilase, in vitro, in silico

  1. S1-2026-493743-abstract.pdf  
  2. S1-2026-493743-bibliography.pdf  
  3. S1-2026-493743-tableofcontent.pdf  
  4. S1-2026-493743-title.pdf