Tripterygium Glycosides

The long-term use of tripterygium glycosides (TG) can lead to male reproductive damage. Research indicates that zinc and selenium exhibit a synergistic effect in the male reproductive system, with the combined preparation demonstrating superior therapeutic effects compared to individual preparations. The purpose of this study was to explore the specific mechanism by which zinc and selenium mitigate reproductive toxicity induced by TG in male rats. Rats were randomly assigned to three groups: control group (C group), model group (M group, receiving TG at 30 mg/kg/day), and model + zinc + selenium group (ZS group). The ZS group was also given TG gavage for the first 4 weeks. Starting from the fifth week until the conclusion of the eighth week, the ZS group received an additional protective treatment of 10 mg/kg/day Zn and 0.1 mg/kg/day Se 4 h after TG administration. Following euthanasia, blood samples, rat testis, and epididymis tissues were collected for further experiments. Combined zinc-selenium treatment corrects the imbalance of zinc-selenium homeostasis in testicular tissue induced by TG. This is achieved by upregulating the expression of metal transcription factor (MTF1) and zinc transporters ZIP8 and ZIP14 and downregulating the expression of ZnT10. Improvement of zinc and selenium homeostasis enhanced the expression of zinc-containing enzymes (ADH, LDH, and ALP) and selenoproteins (GPx1 and SELENOP) in the testis. At the same time, zinc and selenium mitigate TG-induced reproductive damage by promoting the activity of antioxidant enzymes and upregulating the expression of proteins associated with the oxidative stress pathway, including Nrf2, Keap1, HO-1, PI3K, and p-AKT.

This study explored the effect of Tripterygium glycosides(TG) on ulcerative colitis in rats and examined the regulatory role of the extracellular signal-regulated kinase/p38 mitogen-activated protein kinase(ERK/p38 MAPK) signaling pathway. Seventy male Wistar rats were selected and randomly divided into control, model, low-dose TG, medium-dose TG, high-dose TG, positive control, and pathway inhibitor groups. The disease activity index(DAI) score, macroscopic damage score, and microscopic colonic injury score were observed in each group. HE staining was used to detect pathological changes in colonic tissues. TUNEL assay was employed to detect the apoptosis rate of intestinal mucosal cells. ELISA was used to measure serum levels of interleukin-1β(IL-1β), interleukin-6(IL-6), and tumor necrosis factor-alpha(TNF-α). Western blot and PCR methods were used to detect the expression of ERK/p38 MAPK pathway-related proteins and mRNA in tissues. The results showed that TG could effectively improve the histopathological condition; compared with the control group, DAI score, morphological injury score, colon injury score, apoptosis rate of colonic mucosal cells, serum levels of IL-1β, IL-6 and TNF-α, protein levels of p-ERK/ERK and p-p38 MAPK/p38 MAPK, mRNA levels of ERK and p38 MAPK were significantly elevated and significantly increased in the model group(P<0.05). Compared with the model group, DAI scores of rats in the high dose group of TG, the positive control group and the pathway inhibitor group were reduced, and the pathway inhibitor group was the lowest(P<0.05). Compared with the model group, morphological injury score and colonic injury score were reduced in the remaining groups, and lowest in the pathway inhibitor group(P<0.05). Compared with the model group, the apoptosis rate of rat intestinal mucosa cells was decreased in the high-dose TG, the positive control group, and the pathway inhibitor group, and the levels of IL-1β, IL-6, and TNF-α in serum, and the expression of p-ERK/ERK, p-p38 MAPK/p38 MAPK, ERK mRNA, p38 MAPK mRNA in the colonic tissues was reduced(P<0.05), and the improvement effect of the above indexes in the pathway inhibitor group was most significant. In conclusion, TG can effectively improve inflammatory responses in ulcerative colitis, promote colonic mucosal recovery, and enhance immune function. Its mechanism may be related to the regulation of the ERK/p38 MAPK signaling pathway.