Malignant tumors， a group of serious diseases in China， endangers the health of the people. They are mainly treated by surgery， radiotherapy， chemotherapy， targeted therapy， and immunotherapy. With the development of precision medicine， targeted anti-tumor drugs have garnered increasing attention from researchers and gradually applied in clinical treatment. The mitogen-activated protein kinase （MAPK）/nuclear factor-κB （NF-κB） signaling pathway plays a key role in the occurrence and development of tumors， participating in the regulation of tumor microenvironment and the invasion， migration， proliferation， apoptosis， and drug resistance of tumor cells. Therefore， the key effectors targeting the regulation of the MAPK/NF-κB signaling pathway have become potential targets for the treatment of tumors. In China， traditional Chinese medicine （TCM） has become a key approach of tumor treatment since it can exert anti-tumor effects in a multi-component， multi-effect， multi-target， and multi-pathway manner， demonstrating definite clinical efficacy in tumor treatment. The available studies published in recent years have shown that the active components， herb pairs， and compound prescriptions of TCM can play an anti-tumor role by interfering with the MAPK/NF-κB signaling pathway， promoting apoptosis， inhibiting cell proliferation， blocking the cell cycle， inhibiting tumor invasion and metastasis and tumor stem cell characteristics， improving the immune function， and reversing tumor multi-drug resistance. However， a systematic review of the relevant studies remains to be conducted. This paper introduces the mechanism of tumor management via the MAPK/NF-κB pathway and reviews the research progress in TCM treatment of tumors via this pathway in recent years， aiming to provide a theoretical basis for the clinical application of anti-tumor TCM， drug development， and in-depth mechanism research.

OBJECTIVE To investigate the protective effect and mechanism of quercetin on the cardiac and renal functions of rats with cardiorenal syndrome （CRS） based on the phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt）/nuclear factor kappa- B （NF-κB） signaling pathway. METHODS CRS model of SD rats was induced by left anterior descending coronary artery ligation combined with acute renal ischemia-reperfusion. Model rats were randomly separated into model group， quercetin low-dose group （35 mg/kg）， quercetin high-dose group （70 mg/kg）， high-dose of quercetin+740Y-P group （70 mg/kg quercetin+3.5 mg/kg PI3K/Akt/ NF-κB signaling pathway activator 740Y-P）， with 12 rats in each group. Another 12 normal rats were selected as sham operation group. They were given relevant drugs， once a day， for 14 consecutive days. After administration， the cardiac function indexes [left ventricular ejection fraction （LVEF）， end-diastolic volume （EDV）， isovolumic relaxation time （IVRT）] and renal function indicators [blood urea nitrogen （BUN）， 24-hour urine protein， and serum creatinine （Scr）] were detected， and fibrosis in the cardiac and renal tissues was observed； the levels of inflammatory indexes [interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α）] in the serum and cardiac and renal tissues as well as the expression of PI3K/Akt/NF-κB pathway-related proteins in the cardiac and renal tissues were detected. RESULTS Compared with sham operation group， the levels of BUN， 24-hour urine protein and Scr， collagen volume fraction of cardiac and renal tissues， the levels of IL-1β and TNF-α in serum and cardiac and renal tissues， and the phosphorylation of PI3K， Akt and NF-κB p65 protein in cardiac and renal tissues were increased significantly in model group （P＜0.05）； the levels of LVEF， IVRT and EDV were reduced significantly （P＜0.05）. Compared with the model group， the above indexes were reversed significantly in quercetin low-dose and high-dose groups （P＜0.05）， and the reversal effect was better in the high-dose group （P＜0.05）. 740Y-P restored the reverse effect of high-dose quercetin on the indexes （P＜0.05）. CONCLUSIONS Quercetin can alleviate cardiac and renal fibrosis and function injury， the mechanism of which may be 20232016） associated with inhibiting the activation of the PI3K/Akt/NF-κB signaling pathway.

OBJECTIVE To investigate the protective effect and mechanism of cryptotanshinone （CTS） on heart and kidney function in rats with cardiorenal syndrome （CRS） by regulating phosphoinositide kinase-3 （PI3K）/protein kinase B （Akt）/ mammalian target of rapamycin （mTOR） signaling pathway. METHODS CRS model of rats was induced by left anterior descending coronary artery ligation combined with acute renal ischemia-reperfusion injury. Model rats were randomly divided into CRS model group （CRS group）， low-dose CTS group （CTS-L）， high-dose CTS group （CTS-H group）， high-dose CTS+PI3K activator 740Y-P group （CTS-H+740Y-P group）， with 12 rats in each group. Another 12 rats were selected as the normal control group （Normal group） and were carried out surgery without modeling. CTS-L group and CTS-H group were respectively given CTS 30 and 60 mg/kg intragastrically， once a day， for consecutive 14 d. Besides the intervention of CTS 60 mg/kg intragastrically， CTS-H+740Y-P group was given 10 mg/kg 740Y-P intraperitoneally， once a day， for 14 consecutive days. After the last medication， the levels of cardiac function [left ventricular ejection fraction （LVEF）， left ventricular end-systolic diameter （LVESD）， left ventricular end-diastolic diameter （LVEDD）， left ventricular fraction shortening （LVFS）] and renal function [24 h urinary protein， blood urea nitrogen （BUN）， serum creatinine （Scr）， brain natriuretic peptide （BNP）] were detected in rats. The pathological changes and fibrosis of the heart and kidney in rats were observed； the expressions of PI3K/Akt/mTOR signaling pathway in heart and renal tissue were all detected. RESULTS Compared with Normal group， the levels of LVEF and LVFS in rats were all decreased significantly in CRS group （P＜0.05）； the levels of LVESD， LVEDD， 24 h urinary protein， serum levels of BUN， Scr and BNP， collagen area and the phosphorylation of PI3K， Akt and mTOR protein in heart and renal tissue were all increased significantly （P＜0.05）. The morphology of myocardial cells was enlarged and disordered； the structure ofrenal tubules was disordered， epithelial cells were wrinkled， and there was infiltration of inflammatory cells. Compared with CRS group， the above indexes of rats were reversed significantly in CTS-L group and CTS-H group （P＜0.05）； heart and kidney function had been restored， and pathological damage and fibrosis had been reduced. PI3K activator 740Y-P weakened the protective effect of CTS on cardiac and renal function in CRS rats. CONCLUSIONS CTS can protect heart and kidney function in CRS rats， the mechanism of which may be associated with inhibiting the PI3K/Akt/mTOR signaling pathway.