Lotus Seedpod Oligomeric Procyanidin Nanoliposomes Targeting TLR4/NF-κB Reduce Inflammation and Oxidative Stress in Patients with Traumatic Brain Injury

Abstract

The inflammatory-immune response secondary to nerve injury is an important mechanism for craniocerebral injury. Procyanidins from lotus seedpods (LSPCs) are one of the main active ingredients isolated from the mature receptacles of the Nymphaeaceae family lotus plant. LSPCs exhibit strong free radical scavenging and antioxidant activities. The objective of this study was to determine the effects of LSPC nanoliposomes on traumatic brain injury (TBI). In a TBI rat model, LSPC nanoliposomes were injected intraperitoneally. Inflammatory factors and oxidative stress molecules were detected with ELISAs and RT-PCR. The TLR4/NF- κ B signaling pathway was explored using Western blotting. The modified neurological severity scores (mNSS) increased in the TBI group compared with the scores in the Sham group. The water maze test indicated latency in finding the platform was prolonged and staying time in the platform quadrant and the number of times crossing the platform were reduced in the TBI group. Treatment with LSPCs significantly reduced the mNSS scores in rats with TBI and significantly reduced the time to find the platform, increased the residence time in the platform quadrant, and increased the frequency of crossing the platform during the water maze test. In addition, brain edema was reduced in rats with TBI after intraperitoneal injection of LSPCs. Iba-1, IL-1 β , IL-6, and TNF- α levels were reduced after intraperitoneal injection of LSPCs. MDA levels were also reduced, while GSH-Px and SOD levels increased. After intraperitoneal injection of LSPCs, TLR4, MyD88, and pNF- κ B p65 were significantly attenuated. Activation of TLR4 prevented the protective effects of LCPCs in rats with TBI. The results of this study demonstrate that LSPCs attenuate activation of the TLR4/NF- κ B pathway in rats with TBI, thereby reducing microglia activation, inflammation, and oxidative stress.