Salau Veronica F, Erukainure Ochuko L, Koorbanally Neil A, Islam Md Shahidul
Department of Biochemistry, University of KwaZulu-Natal (Westville Campus), Durban, South Africa.
Department of Biochemistry, Veritas University, Bwari, Abuja, Nigeria.
J Food Biochem. 2022 Apr;46(4):e13641. doi: 10.1111/jfbc.13641. Epub 2021 Feb 8.
The antidiabetic properties of ferulic acid and its protective role against Fe -induced oxidative pancreatic injury were investigated in this study using in vitro and ex vivo models. Induction of oxidative injury in the pancreas was achieved by incubating normal pancreatic tissue with 0.1 mM FeSO and treated by co-incubating with different concentrations of ferulic acid for 30 min at 37°C. Ferulic acid inhibited the activities of α-glucosidase, α-amylase, and pancreatic lipase significantly (p < .05) and promoted glucose uptake in isolated rat psoas muscles. Induction of oxidative pancreatic injury caused significant (p < .05) depletion of glutathione (GSH) level, superoxide dismutase (SOD), and catalase activities, as well as elevation of malondialdehyde (MDA) and nitric oxide (NO) levels, acetylcholinesterase and chymotrypsin activities. Treatment of tissues with ferulic acid significantly (p < .05) reversed these levels and activities. LC-MS analysis of the extracted metabolites revealed 25% depletion of the normal metabolites with concomitant generation of m-Chlorohippuric acid, triglyceride, fructose 1,6-bisphosphate, and ganglioside GM1 in oxidative-injured pancreatic tissues. Treatment with ferulic acid restored uridine diphosphate glucuronic acid and adenosine tetraphosphate and generated P1,P4-Bis(5'-uridyl) tetraphosphate and L-Homocysteic acid, while totally inactivating oxidative-generated metabolites. Ferulic acid also inactivated oxidative-activated pathways, with concomitant reactivation of nucleotide sugars metabolism, starch and sucrose metabolism, and rostenedione metabolism, estrone metabolism, androgen and estrogen metabolism, porphyrin metabolism, and purine metabolism pathways. Taken together, our results indicate the antidiabetic and protective potential of ferulic acid as depicted by its ability to facilitate muscle glucose uptake, inhibit carbohydrate and lipid hydrolyzing enzymes, and modulate oxidative-mediated dysregulated metabolisms. PRACTICAL APPLICATIONS: There have been increasing concerns on the side effects associated with the use of synthetic antidiabetic drug, coupled with their expenses particularly in developing countries. This has necessitated continuous search for alternative treatments especially from natural products having less or no side effects and are readily available. Ferulic acid is among the common phenolics commonly found in fruits and vegetables. In this present study, ferulic acid was able to attenuate oxidative stress, cholinergic dysfunction, and proteolysis in oxidative pancreatic injury, as well as inhibit carbohydrate digesting enzymes. Thus, indicating the ability of the phenolic to protect against complications linked to diabetes. Crops rich in ferulic acid maybe beneficial in managing this disease.
本研究使用体外和离体模型,对阿魏酸的抗糖尿病特性及其对铁诱导的胰腺氧化损伤的保护作用进行了研究。通过将正常胰腺组织与0.1 mM硫酸亚铁孵育来诱导胰腺氧化损伤,并在37°C下与不同浓度的阿魏酸共同孵育30分钟进行处理。阿魏酸显著抑制了α-葡萄糖苷酶、α-淀粉酶和胰腺脂肪酶的活性(p < 0.05),并促进了离体大鼠腰大肌对葡萄糖的摄取。胰腺氧化损伤的诱导导致谷胱甘肽(GSH)水平、超氧化物歧化酶(SOD)和过氧化氢酶活性显著降低(p < 0.05),同时丙二醛(MDA)和一氧化氮(NO)水平、乙酰胆碱酯酶和胰凝乳蛋白酶活性升高。用阿魏酸处理组织显著(p < 0.05)逆转了这些水平和活性。对提取的代谢物进行液相色谱-质谱分析显示,氧化损伤的胰腺组织中正常代谢物减少了25%,同时生成了间氯马尿酸、甘油三酯、果糖1,6-二磷酸和神经节苷脂GM1。用阿魏酸处理可恢复尿苷二磷酸葡萄糖醛酸和四磷酸腺苷,并生成P1,P4-双(5'-尿苷基)四磷酸和L-高半胱氨酸,同时完全使氧化产生的代谢物失活。阿魏酸还使氧化激活的途径失活,同时使核苷酸糖代谢、淀粉和蔗糖代谢以及雄烯二酮代谢、雌酮代谢、雄激素和雌激素代谢、卟啉代谢和嘌呤代谢途径重新激活。综上所述,我们的结果表明,阿魏酸具有抗糖尿病和保护潜力,其表现为促进肌肉对葡萄糖的摄取、抑制碳水化合物和脂质水解酶以及调节氧化介导的代谢失调。实际应用:人们越来越关注合成抗糖尿病药物的副作用及其费用,特别是在发展中国家。这就需要不断寻找替代治疗方法,尤其是来自副作用较少或无副作用且容易获得的天然产物。阿魏酸是水果和蔬菜中常见的酚类物质之一。在本研究中,阿魏酸能够减轻胰腺氧化损伤中的氧化应激、胆碱能功能障碍和蛋白水解作用,以及抑制碳水化合物消化酶。因此,表明这种酚类物质能够预防与糖尿病相关的并发症。富含阿魏酸的作物可能对控制这种疾病有益。