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Key message: Compared with NaCl, NaHCO3 caused more serious oxidative damage and photosynthesis inhibition in safflower by down-regulating the expression of related genes. Salt-alkali stress is one of the important factors that limit plant growth. NaCl and sodium bicarbonate (NaHCO3) are neutral and alkaline salts, respectively. This study investigated the physiological characteristics and molecular responses of safflower (Carthamus tinctorius L.) leaves treated with 200 mmol L−1 of NaCl or NaHCO3. The plants treated with NaCl treatment were less effective at inhibiting the growth of safflower, but increased the content of malondialdehyde (MDA) in leaves. Meanwhile, safflower alleviated stress damage by increasing proline (Pro), soluble protein (SP), and soluble sugar (SS). Both fresh weight and dry weight of safflower was severely decreased when it was subjected to NaHCO3 stress, and there was a significant increase in the permeability of cell membranes and the contents of osmotic regulatory substances. An enrichment analysis of the differentially expressed genes (DEGs) using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes identified significant enrichment of photosynthesis and pathways related to oxidative stress. Furthermore, a weighted gene co-expression network analysis (WGCNA) showed that the darkgreen module had the highest correlation with photosynthesis and oxidative stress traits. Large numbers of transcription factors, primarily from the MYB, GRAS, WRKY, and C2H2 families, were predicted from the genes within the darkgreen module. An analysis of physiological indicators and DEGs, it was found that under saline-alkali stress, genes related to chlorophyll synthesis enzymes were downregulated, while those related to degradation were upregulated, resulting in inhibited chlorophyll biosynthesis and decreased chlorophyll content. Additionally, NaCl and NaHCO3 stress downregulated the expression of genes related to the Calvin cycle, photosynthetic antenna proteins, and the activity of photosynthetic reaction centers to varying degrees, hindering the photosynthetic electron transfer process, suppressing photosynthesis, with NaHCO3 stress causing more pronounced adverse effects. In terms of oxidative stress, the level of reactive oxygen species (ROS) did not change significantly under the NaCl treatment, but the contents of hydrogen peroxide and the rate of production of superoxide anions increased significantly under NaHCO3 stress. In addition, treatment with NaCl upregulated the levels of expression of the key genes for superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), the ascorbate-glutathione cycle, and the thioredoxin-peroxiredoxin pathway, and increased the activity of these enzymes, thus, reducing oxidative damage. Similarly, NaHCO3 stress increased the activities of SOD, CAT, and POD and the content of ascorbic acid and initiated the glutathione-S-transferase pathway to remove excess ROS but suppressed the regeneration of glutathione and the activity of peroxiredoxin. Overall, both neutral and alkaline salts inhibited the photosynthetic process of safflower, although alkaline salt caused a higher level of stress than neutral salt. Safflower alleviated the oxidative damage induced by stress by regulating its antioxidant system. [ABSTRACT FROM AUTHOR]

Objective: C1q/tumour necrosis factor-related protein 12 (CTRP12) is closely related to coronary artery disease and has an outstanding cardioprotective effect. However, whether CTRP12 participates in heart failure (HF) has not been well studied. This work aimed to explore the role and mechanism of CTRP12 in post-myocardial infarction (MI) HF. Methods: Rats were subjected to left anterior descending artery ligation and then raised for six weeks to establish post-MI HF. Recombinant adeno-associated virus-mediated gene transfer was applied to overexpress or silence CTRP12 in rat hearts. RT-qPCR, Immunoblot, Echocardiography, Haematoxylin–eosin (HE) staining, Masson's trichrome staining, TUNEL staining and ELISA were carried out. Results: CTRP12 levels were decreased in the hearts of rats with post-MI HF. The overexpression of CTRP12 improved cardiac function and attenuated cardiac hypertrophy and fibrosis in rats with post-MI HF. CTRP12 silencing exacerbated cardiac dysfunction, hypertrophy and fibrosis in rats with post-MI HF. The cardiac apoptosis, oxidative stress and inflammatory response induced by post-MI HF were weakened by CTRP12 overexpression or aggravated by CTRP12 silencing. CTRP12 inhibited the activation of the transforming growth factor‐β activated kinase 1 (TAK1)-p38 mitogen‐activated protein kinase (MAPK)/c‐Jun N‐terminal kinase (JNK) pathway in the hearts of rats with post-MI HF. Treatment with the TAK1 inhibitor reversed the adverse effects of CTRP12 silencing on post-MI HF. Conclusions: CTRP12 protects against post-MI HF by modulating the TAK1-p38 MAPK/JNK pathway. CTRP12 may be a therapeutic target for the treatment of post-MI HF. [ABSTRACT FROM AUTHOR]