School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung 404, Taiwan.
Chinese Medicine Research Center, China Medical University, Taichung 404, Taiwan.
Nutrients. 2024 Oct 18;16(20):3532. doi: 10.3390/nu16203532.
BACKGROUND/OBJECTIVES: Acute kidney injury (AKI) syndrome is distinguished by a quick decline in renal excretory capacity and usually diagnosed by the presence of elevated nitrogen metabolism end products and/or diminished urine output. AKI frequently occurs in hospital patients, and there are no existing specific treatments available to diminish its occurrence or expedite recovery. For an extended period in the food industry, has been distinguished by its robust bacteriocin production, effectively inhibiting pathogen growth during fermentation and storage.
In this study, the aim is to assess the effectiveness of GKA4, dead probiotic GKA4, and postbiotic GKA4 against cisplatin-induced AKI in an animal model. The experimental protocol involves a ten-day oral administration of GKA4, dead probiotic GKA4, and postbiotic GKA4 to mice, with a cisplatin intraperitoneal injection being given on the seventh day to induce AKI.
The findings indicated the significant alleviation of the renal histopathological changes and serum biomarkers of GKA4, dead probiotic GKA4, and postbiotic GKA4 in cisplatin-induced nephrotoxicity. GKA4, dead probiotic GKA4, and postbiotic GKA4 elevated the expression levels of HO-1 and decreased the expression levels of Nrf-2 proteins. In addition, the administration of GKA4, dead probiotic GKA4, and postbiotic GKA4 significantly reduced the expression of apoptosis-related proteins (Bax, Bcl-2, and caspase 3), autophagy-related proteins (LC3B, p62, and Beclin1), and endoplasmic reticulum (ER) stress-related proteins (GRP78, PERK, ATF-6, IRE1, CHOP, and Caspase 12) in kidney tissues. Notably, GKA4, dead probiotic GKA4, and postbiotic GKA4 also upregulated the levels of proteins related to organic anion transporters and organic cation transporters.
Overall, the potential therapeutic benefits of GKA4, dead probiotic GKA4, and postbiotic GKA4 are significant, particularly after cisplatin treatment. This is achieved by modulating apoptosis, autophagy, ER stress, and transporter proteins to alleviate oxidative stress.
背景/目的：急性肾损伤（AKI）综合征的特点是肾脏排泄能力迅速下降，通常通过升高的氮代谢终产物和/或减少的尿量来诊断。AKI 在住院患者中经常发生，目前尚无特定的治疗方法可以减少其发生或促进其恢复。在食品工业中，已经有很长一段时间因其强大的细菌素生产能力而脱颖而出，在发酵和储存过程中有效抑制病原体的生长。
本研究旨在评估 GKA4、死益生菌 GKA4 和后生元 GKA4 对动物模型中顺铂诱导的 AKI 的疗效。实验方案包括用 GKA4、死益生菌 GKA4 和后生元 GKA4 对小鼠进行十天的口服给药，第七天给予顺铂腹腔注射以诱导 AKI。
研究结果表明，GKA4、死益生菌 GKA4 和后生元 GKA4 对顺铂诱导的肾毒性具有显著的缓解作用，减轻了肾组织病理学变化和血清生物标志物。GKA4、死益生菌 GKA4 和后生元 GKA4 上调了 HO-1 的表达水平，降低了 Nrf-2 蛋白的表达水平。此外，GKA4、死益生菌 GKA4 和后生元 GKA4 的给药显著降低了凋亡相关蛋白（Bax、Bcl-2 和 caspase 3）、自噬相关蛋白（LC3B、p62 和 Beclin1）和内质网（ER）应激相关蛋白（GRP78、PERK、ATF-6、IRE1、CHOP 和 Caspase 12）在肾脏组织中的表达。值得注意的是，GKA4、死益生菌 GKA4 和后生元 GKA4 还上调了有机阴离子转运体和有机阳离子转运体相关蛋白的水平。
总的来说，GKA4、死益生菌 GKA4 和后生元 GKA4 的潜在治疗益处是显著的，特别是在顺铂治疗后。这是通过调节凋亡、自噬、内质网应激和转运蛋白来减轻氧化应激实现的。
