ObjectiveTo investigate the effect of Curcumin combined with Rhodiola on rats with severe acute pancreatitis (SAP) associated renal injury and explore the possible mechanisms. MethodsA total of 24 rats were randomly divided into SAP with renal injury group (SAP group, n=8), Curcumin group (n=8), Curcumin combined with Rhodiola group (n=8).The SAP group was given 1.5 mL saline through intragastric administration before operation while the Curcumin group was fed with same amount of Curcumin diluent.The Curcumin combined with Rhodiola group was given 1.5 mL Curcumin diluent through intragastric administration and 6 g/kg Rhodiola diluent through intraperitoneal injection before operation.The pancreas and pancreatic tail-segment was dissociated and the head of pancreas were occluded in rats to make the model, blood vessel forceps was loosed after three hours.All the rats were sacrificed at 18 h after modeling.The levels of serum amylase, creatinine, blood urea nitrogen were detected and pathological changes of pancreas and the left kidney were observed under the light microscope.The cell apoptosis was analyzed using TUNEL staining.The serum levels of interleukin (IL)-1β, IL-6, and IL-10 among the three groups were detected by enzyme-linked immunosorbent assay.The expression of inducible nitric oxide synthase (iNOS) mRNA in the right kidney was detected by real-time polymerase chain reaction.The superoxide dismutase (SOD) activity of the renal tissue was determined by hydroxylamine method. ResultsCompared with the SAP group, the levels of serum amylase, creatinine, blood urea nitrogen, IL-1β, IL-6, the cell apoptosis index, and the expression of iNOS mRNA were significantly decreased, the serum level of IL-10 and the activity of SOD were significantly increased (P < 0.05), the pancreas and the kidney damaged more slightly in the Curcumin group and Curcumin combined with Rhodiola group.Compared with the Curcumin group, the above situations were more better in the Curcumin combined with Rhodiola group. ConclusionsCurcumin combined with Rhodiola has a better protective effect on SAP associated renal injury.It might be through inhibiting the expressions of IL-1β, IL-6, stimulating the expression of IL-10, down-regulating the expression of iNOS mRNA, and improving the activity of SOD.It could reduce the cell apoptosis and necrosis of the kidney and improve the ability of the kidney to tolerate hypoxia.
ObjectiveTo investigate the expression of connective tissue growth factor (CTGF) in the chronic sciatic nerve compression injury and to explore the effect of rhodiola sachalinensis on the expression of CTGF. MethodsForty-five adult male Sprague Dawley rats were randomly divided into groups A, B, and C:In group A (sham-operated group), only the sciatic nerve was exposed; in group B (compression group), sciatic nerve entrapment operation was performed on the right hind leg according to Mackinnon method to establish the chronic sciatic nerve compression model; and in group C (compression and rhodiola sachalinensis group), the sciatic nerve entrapment operation was performed on the right hind leg and rhodiola sachalinensis (2 g/mL) was given by gavage at a dose of 0.5 mL/100 g for 2 weeks. The nerve function index (SFI) was observed and neural electrophysiology was performed; histology, transmission electron microscope, real-time fluorescent quantitative PCR, and Western blot were performed to observe the morphological changes of the compressed nerve tissue and to determine the mRNA and protein levels of CTGF, collagen type I, and collagen type Ⅲ at 2, 6, and 10 weeks after operation. ResultsAt 6 and 10 weeks after operation, SFI of groups A and C were significantly better than that of group B (P < 0.05), but there was no significant difference between groups A and C (P > 0.05). The nerve function test showed that the nerve motor conduction velocity (MCV) and the amplitude of compound muscle action potential (CMAP) of group B were significantly lower than those of groups A and C, and distal motor latency (DML) was significantly prolonged in group B (P < 0.05), but there was no significant difference between groups A and C (P > 0.05). Histology and transmission electron microscope observations showed that myelinated nerve fibers degenerated and collagen fiber hyperplasia after sciatic nerve chronic injury in group B, and rhodiola sachalinensis could promote the repair of nerve fibers in group C. At 2 weeks postoperatively, the number of myelinated nerve fibers in groups B and C were significantly less than that of group A (P < 0.05), and the myelin sheath thickness of groups B and C were significantly larger than that of group A (P < 0.05). At 6 and 10 weeks postoperatively, the number of myelinated nerve fibers in groups B and C were significantly more than that of group A (P < 0.05); the myelin sheath thickness of group B was significantly less than that of groups A and C (P < 0.05). The effective area of nerve fiber had no significant difference among groups at each time point (P > 0.05). Real-time fluorescent quantitative PCR and Western blot results showed that the mRNA and protein expressions of CTGF, collagen type I, and collagen type Ⅲ in group B were significantly higher than those in groups A and C at each time point (P < 0.05), but there was no significant difference between groups A and C (P > 0.05). ConclusionSciatic nerve fibrosis can be caused by chronic nerve compression. The increased expression of CTGF suggests that CTGF plays an important role in the process of neural injury and fibrosis. Rhodiola sachalinensis can significantly reduce the level of CTGF and plays an important role in nerve functional recovery.
Objective To explore the potential molecular mechanism of Rhodiola crenulata (RC) for type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD) by network pharmacology and molecular docking. Methods The target genes of T2DM and AD, the effective active components and targets of RC were identified through multiple public databases during March to August, 2022. The main active components and core genes of RC anti T2DM-AD were screened. The key genes were enrichment analyzed by gene ontology function and Kyoto gene and Kyoto Encyclopedia of Genes and Genomes. AutoDock Vina was used for molecular docking and binding energy calculation. Results A total of 5189 T2DM related genes and 1911 AD related genes were obtained, and the intersection result showed that there were 1418 T2DM-AD related genes. There were 48 active components of RC and 617 corresponding target genes. There were 220 crossing genes between RC and T2DM-AD. The main active components of RC anti T2DM-AD included kaempferol, velutin, and crenulatin. The key genes for regulation include ESR1, EGFR, and AKT1, which were mainly enriched in the hypoxia-inducible factor-1 signal pathway, estrogen signal pathway, and vascular endothelial growth factor signal pathway. The docking binding energies of the main active components of RC and key gene molecules were all less than −1.2 kcal/mol (1 kcal=4.2 kJ). Conclusions RC may play a role in influencing T2DM and AD by regulating the hypoxia-inducible factor-1 signaling pathway, estrogen signaling pathway, and vascular endothelial growth factor signaling pathway.