Lycopene (LYC) is a carotenoid, has antioxidant properties. This study investigated whether lycopene attenuates aristolochic acids (AAs) -induced chronic kidney disease. In this experiment, lycopene was used to intervene C57BL/6 mice with renal injury induced by aristolochic acid exposure. The histomorphological changes and serological parameters of the kidney were measured in order to assess the alleviating effect of lycopene on renal injury in aristolochic acid nephropathy. In vitro and in vivo experiments were carried out to verify the main mechanism of action and drug targets of lycopene in improving aristolochic acid nephropathy (AAN) and by various experimental methods such as ELISA, immunohistochemistry, immunofluorescence, Western-blot and qRT-PCR. The results showed that oxidative stress injury was induced in the kidney of mice after AAI exposure, resulting in inflammatory response and tubular epithelial cell apoptosis. The results showed that the Nrf2/HO-1 antioxidant signaling pathway was inhibited after AAI exposure. AAI induces oxidative stress injury in the kidney, which ultimately leads to inflammation and tubular epithelial cell apoptosis. After LYC intervened in the body, it activated Nrf2 nuclear translocation and its downstream HO-1 and NQO1 antioxidant signaling pathways. LYC inhibited ROS production by renal tubular epithelial cells, and alleviated mitochondrial damage. LYC further modulated the TNF-α/NF-κB signaling cascade, thereby reduced the accumulation of inflammatory factors in the renal interstitium. Moreover, LYC was able to up-regulate the expression of Bcl-2, down-regulate Bax expression and inhibit the activation of cleaved forms of Caspase-9 and Caspase-3, which finally attenuated the apoptosis of the mitochondrial pathway induced by AAI exposure. It was concluded that lycopene was able to activate the Nrf2 antioxidant signaling pathway to maintain the homeostasis of renal oxidative stress and ultimately attenuated renal inflammatory response and apoptosis. These results suggested that lycopene can be used as a drug to relieve AAN.

Aristolochic acid (AA) are persistent soil pollutants in the agricultural fields of the Balkan Peninsula. Preparations containing aristolochic acid are widely used for anti-inflammatory, diuretic, etc. To study the hepatotoxicity of aristolochic acid, 80 healthy SD rats were selected and divided into 20 mg/kg- AA group, 4 mg/kg-AA group, and 2 mg/kg-AA group and blank group, 20 rats per group. Mainly tested the body weight, liver function, liver tissue oxidative stress and pathological changes of liver tissue in rats. The ALT and AST activities in the serum of the rats in the administration groups were increased compared with the blank group. The activity of MDA in the administration groups was higher than that in the blank group; the activities of SOD, T-AOC and GSH-PX were significantly lower than those in the blank group. HE tissue sections also found that the administration groups showed varying degrees of hepatocyte boundary blur, nuclear fragmentation, and fibrosis tendency. Transmission electron microscopy showed that the mitochondria of the rat liver became more and more severely damaged with the increase of dose. Compared with the blank group, the mRNA expression of Bax, Caspase-9 and Caspase-3 in the administration groups were determined, while the mRNA expression of the Bcl-2 was increased. And compared with the blank control group, the expression levels of apoptotic proteins caspase-9 and caspase-3 increased significantly in the 20 mg/kg-AA group. Aristolochic acid can induce liver injury in rats through oxidative stress pathway and mitochondrial apoptosis pathway.

Background: Inhibiting secondary inflammatory damage caused by glial cells and creating a stable microenvironment is one of the main strategies to investigate drugs for the treatment of spinal cord injury. Acetyl‐11‐keto‐beta‐boswellic acid (AKBA) is the active component of the natural drug boswellia, which has anti‐inflammatory and antioxidant effects and offers a possible therapeutic option for spinal cord injury.Methods: In this study, a spinal cord injury model was established by crushing spinal cord, respectively, to detect the M1 macrophage inflammatory markers: iNOS, TNF‐α, IL‐1β, and the M2 macrophage markers CD206, ARG‐1, IL‐10, and the detection of antioxidant enzymes and MDA. In vitro, macrophages were cultured to verify the main mechanism of the macrophage switch from Nrf2/HO‐1 to M2 type by flow cytometry, immunofluorescence, and other techniques. Macrophage and Schwann cell co‐culture validated the migration mechanism of Schwann cells promoted by AKBA.Results: AKBA significantly enhanced the antioxidant enzyme activities of CAT, GSH‐Px, T‐AOC, and SOD, reduced MDA content, and reduced oxidative damage caused by spinal cord injury via the Nrf2/HO‐1 signaling pathway; AKBA mediates Nrf2/HO‐1/IL‐10, converts macrophages from M1 to M2 type, reduces inflammation, and promotes Schwann cell migration, thereby accelerating the repair of spinal cord injury in rats.Conclusions: Our work demonstrates that AKBA can attenuate oxidative stress as well as the secondary inflammatory injury caused by macrophages after SCI, promote Schwann cell migration to the injury site, and thus accelerate the repair of the injured spinal cord.

Dracorhodin perchlorate (DP) is extracted from Dragon’s blood, which is widely used in traditional Chinese medicine, especially in wound healing. The aim of this paper is to investigate the influence of DP ointment, which contained DP dissolved in DMSO and mixed with Vaseline, on cutaneous wound healing in Wistar rats. Forty Wistar rats were divided into two groups: control and DP groups. The skin on the back of each rat was punched with two full‐thickness wounds and then treated with the corresponding drug. After 3, 7, 10, 14, and 21 days, four rats were sacrificed for immunological, biochemical, and histological analyses. Compared with the control treatment, DP could significantly promote wound closure. Histological and biochemical analyses of the skin biopsies also showed that DP regulated the expression of inflammatory responses by TNF‐α and IL‐β and by supporting wound tissue growth and collagen deposition. Western blot revealed that DP could also facilitate the expression of EGF and VEGF proteins. In conclusion, DP promotes wound healing.