Paeoniflorin (PF) has been reported to possess neuroprotective influences on cognitive dysfunction illness. In current research, we attempted to probe into the protective influences of PF against H₂O₂-induced damage and the underlying regulating mechanisms on hippocampal HT-22 cells. HT-22 cells were pretreated with PF, and then induced by H₂O₂. Afterwards, the influences of PF pretreatment were examined using CCK-8 assay, apoptosis assay, western blot and ROS assay, respectively. In addition, the expression of microRNA-135a (miR-135a) was analyzed and altered by qRT-PCR and cell transfection, respectively. After overexpression of miR-135a, the effects of miR-135a mimic on cell functions were detected again. Moreover, influences of H₂O₂, PF and miR-135a overexpression on JAK2/STAT3 and ERK1/2 signal pathways were further investigated. Further experiments verified that PF pretreatment alleviated H₂O₂-induced oxidative stress through increasing cell viability, inhibiting cell apoptosis, reducing ROS generation and activating JAK2/STAT3 and ERK1/2 pathways. Besides, expression of miR-135a was declined by PF pretreatment. Whereas, miR-135a mimic abrogated the protective effects triggered by PF pretreatment. These results indicated that PF can alleviate H₂O₂-induced oxidative stress by down-regulation of miR-135a via activation of JAK2/STAT3 and ERK1/2 pathways.

据报道药苷（PF）对认知功能障碍疾病具有神经保护作用。在当前的研究中，我们试图探讨PF对H ₂ O ₂诱导的损伤的保护作用及其对海马HT-22细胞的潜在调节机制。HT-22细胞用PF预处理，然后被H ₂ O ₂诱导。然后，分别用CCK-8法，凋亡法，western blot法和ROS法检测了PF预处理的影响。另外，分别通过qRT-PCR和细胞转染来分析和改变microRNA-135a（miR-135a）的表达。miR-135a过表达后，再次检测到miR-135a模拟物对细胞功能的影响。而且，H的影响_{进一步研究了2} O ₂，PF和miR-135a在JAK2 / STAT3和ERK1 / 2信号通路上的过表达。进一步的实验证明，PF预处理可通过增加细胞活力，抑制细胞凋亡，减少ROS生成并激活JAK2 / STAT3和ERK1 / 2途径减轻H ₂ O ₂诱导的氧化应激。此外，PF预处理降低了miR-135a的表达。而miR-135a模拟物取消了PF预处理触发的保护作用。这些结果表明，PF可以通过激活JAK2 / STAT3和ERK1 / 2途径下调miR-135a来减轻H ₂ O ₂引起的氧化应激。