[Pathogenesis of ferroptosis on chronic kidney disease and traditional Chinese medicine intervention: a review].

Chronic kidney disease(CKD) is an insidious disease that has become a significant global public health issue due to its high incidence rate, low awareness, low diagnostic rate, poor prognosis, and high medical costs. Recent studies have shown that CKD development is associated with varying degrees of ferroptosis features. Traditional Chinese medicine(TCM) can regulate iron metabolism, lipid peroxidation, antioxidant systems to inhibit ferroptosis and delay the progression of CKD. Consequently, the intervention mechanism of ferroptosis has become one of the focuses of CKD research. TCM has thousands of years of traditional experience and wisdom. It focuses on the overall regulation of human body functions and can stimulate the body's disease resistance and recovery capabilities, which has certain advantages in treating CKD. However, there is currently a lack of comprehensive articles on the application of TCM in intervening ferroptosis to treat CKD and the pathogenesis of ferroptosis in CKD. Therefore, this article summarizes the latest research progress both domestically and internationally, briefly introduces the main mechanisms of ferroptosis, and systematically reviews the relationship between ferroptosis and CKD. The article integrates TCM theories related to ferroptosis in CKD, including "deficiency" "stasis" "phlegm turbidity" and "toxins" and summarizes the research status of active ingredients and herbal formulas in intervening ferroptosis to treat CKD. By considering ferroptosis from a new perspective, this article aims to provide new targets and directions for the application of TCM in treating CKD.

[Protective effects of shenmai injection on the delayed injury of the cerebral neurons in rat induced by intracerebral hemorrhage].

OBJECTIVE: To observe protective effects of Shenmai (SM) injection on the delayed injury of the cerebral neurons in rat with intracerebral hemorrhage. METHOD: Rosenberg models of intracerebral hemorrhage was established and the effects of SM injection on the pathologic changes in neuronal structure, mitochondria-DNA(mtDNA)deletion, C-myc gene and expression PDGF-A gene in hippocampal CA1 areas, were investigated. RESULT: SM injection inhibited the apoptosis of pyramidal cells in the hippocampal CA1 areas, and decreased the degree of mtDNA deletion in the neurons in the injured area. SM injection had no effect on gene expression of C-myc at initial stage a intracerebral hemorrhage, but significantiy decreased the level of PDGF-A mRNA and prolonged the time of its expression. CONCLUSION: SM injection might attenuate the delayed injury induced by intracerebral hemorrhage via regulating the expression of PDGF.