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Objective@#To explore the protective effect and mechanism of Somatostatin (SS) on the mice with Paraquat (PQ) poisoning, and to provide theoretical basis for clinical treatment of PQ poisoning.@*Methods@#48 SPF male BALB/c mice were randomly divided into control group, SS group, PQ group and PQ+SS group, with 12 mice in each group. 20 ml/kg SS solution was intraperitoneally injected into the SS group and PQ+SS group, and the same amount of normal saline was intraperitoneally injected into the PQ group and control group. After 1 hour of the above treatment, PQ group and PQ+SS group were given 60 mg/kg PQ solution by one-time gavage, while the control group and SS group were given the same amount of normal saline by gavage. After the above treatment for 3 hours, the SS group and PQ+SS group were intraperitoneally injected with SS solution (20 ml/kg) again, and the PQ group and the control group were intraperitoneally injected with the same amount of normal saline. 6 eyeballs were randomly selected from each group for blood collection, and the levels of TNF-α, MPO and il-6 in the blood of mice were detected by ELISA and other methods. The left lung was taken after blood collection to calculate the D/W ratio. The levels of SOD, caspase-3 and MDA were detected in some lung tissues by chemical colorimetry, and the amount of NF-κB was detected by Western blot. The lung histopathological changes were observed under light microscope.@*Results@#The mice in the control group and SS group showed normal activity and good general condition; Mice in the PQ group ate less and moved less, responded slowly to stimulation, breathed shallow and fast with thickened breath sound, had messy and dull fur, and had varying degrees of cyanosis on their lips and limbs; The above performance of PQ+SS group was less than that of PQ group. Under the light microscope, the alveolar structure of PQ group was disordered and seriously damaged. The pathological changes of lung tissue in PQ+SS group were significantly improved compared with that in PQ group, and the pathological scores were decreased (all P<0.05) . Compared with the control group, there was no significant change in the levels of various indicators in the SS group (all P>0.05) . While the levels of inflammatory cytokines (IL-6, TNF-α, Protein expression of NF-κB) , oxidative cytokines (MPO, MDA) and apoptotic cytokines caspase-3 in PQ mice were significantly increased, and the levels of oxidative cytokines SOD and lung tissue D/W were significantly decreased (all P<0.05) . Compared with the PQ group, the PQ+SS group, the levels of inflammatory cytokines (IL-6, TNF-α, Protein expression of NF-κB) , oxidative cytokines (MPO, MDA) and apoptotic cytokines caspase-3 decreased, and the levels of oxidative cytokines SOD and lung tissue D/W increased (all P<0.05) .@*Conclusion@#PQ poisoning can cause lung injury in mice, while SS can alleviate lung injury in PQ poisoned mice, improve the general survival state of mice, and play a certain protective role in lung injury caused by PQ poisoning, which may be achieved by SS throμgh reducing the inflammatory response, oxidative stress response and lung tissue apoptosis in lung injury caused by PQ poisoning.
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Objective@#To investigate the effects of mono-carbonyl analogues of curcumin (L6H21) on paraquat (PQ) -induced injury in HK-2 cell line and explore its underlying mechanisms.@*Methods@#Cultured HK-2 cells were challenged by PQ with or without L6H21 treatment. Cell viability and apoptosis were determined by CCK-8 assay and flow cytometry, respectively. Gene expressions and protein levels of apoptotic and inflammatory factors were assessed by RT-PCR, ELISA, and western blot. Intracellular ROS production was detected by DCFH-DA staining. Superoxide dismutase (SOD) and malondialdehyde (MDA) were examined by chemical colorimetry.@*Results@#1) PQ challenge significantly inhibited HK-2 cells proliferation, which was prevented by L6H21 administration. PQ dramatically induced HK-2 apoptosis evidenced by increasing expressions of caspase-9, caspase-3 and Bax, while decreasing Bcl-2 level. However, PQ induced these apoptotic effects in HK-2 cells were reversed by L6H21. Similarly, PQ exposure obviously enhanced activity of NF-κB and levels of cytokines (TNF-α、IL-6) in HK-2 cells, which was inhibited by L6H21. Furthermore, administration of L6H21 inhibited PQ induced ROS and MDA production, and promoted SOD level in HK-2 cells.@*Conclusion@#L6H21 administration inhibits PQ-induced apoptosis in HK-2 cells possibly by reducing inflammation and oxidative damage.