Objective To explore the effects of STAT1 on apoptosis of rat macrophages and MAPK/NF-κB signaling pathway in pulmonary tuberculosis.Methods Forty rats were randomly divided into four groups,includ-ing the control group,PTB group,STAT1-ASO group,and STAT1-ASO+Anisomycin group,with 10 rats in each group.The number of Mycobacterium tuberculosis colonies in lung tissues was counted.Bronchoalveolar lavage macro-phages were collected,and apoptosis of lung tissue macrophages was detected by flow cytometry.Lung tissue histo-pathological changes were examined by HE staining.The levels of IL-6,IL-1β,and TNF-α in serum were measured by ELISA.The levels of SOD and MDA in lung tissues were determined.Protein expression of p38 MAPK,p-p38 MAPK,p65 NF-κB,and p-p65 NF-κB in wound tissue was detected by Western blotting.Results Compared with the control group,the TB group showed significant increases in the number of Mycobacterium tuberculosis colonies(9.12±0.81),macrophage apoptosis rate(51.27±4.16),serum IL-6(215.42±15.33),IL-1β(73.62±6.04),TNF-α(81.24±5.79)levels,lung tissue MDA content(9.54±1.72),and p-p38 MAPK/p38 MAPK ratio(0.92±0.12),as well as p-p65 NF-KB/p65 NF-κB ratio(0.87±0.10),while pulmonary SOD activity(31.27±2.85)was significantly decreased(P＜0.05).Compared with the TB group,the STAT1-ASO group showed significant decreases in the num-ber of M.tuberculosis colonies(3.87±0.40),macrophage apoptosis rate(8.91±0.43),serum IL-6(40.91±3.46),IL-1β(21.54±1.79),TNF-α(20.35±1.87)levels,lung tissue MDA content(2.69±0.72),and p-p38 MAPK/p38 MAPK ratio(0.45±0.07),as well as p-p65 NF-KB/p65 NF-κB ratio(0.39±0.06),while pulmonary SOD activity(72.15±6.81)was significantly increased(P＜0.05).Compared with the STAT1-ASO group,the STAT1-ASO+Aniso-mycin group showed significant increases in the number of Mycobacterium tuberculosis colonies(8.75±0.74),macro-phage apoptosis rate(42.86±3.75),serum IL-6(192.11±13.61),IL-1 β(67.33±5.24),TNF-α(75.26±5.11)lev-els,lung tissue MDA content(9.01±1.65),and p-p38 MAPK/p38 MAPK ratio(0.87±0.10),as well as p-p65 NF-κB/p65 NF-κB ratio(0.80±0.09),while pulmonary SOD activity(36.49±3.01)was significantly decreased(P＜0.05).Conclusion Inhibition of STAT1 activation can suppress the inflammatory response and improve lung tissue damage in rats with pulmonary tuberculosis.It also inhibits macrophage apoptosis in lung tissues,and its mechanism of action may be related to the inhibition of MAPK/NF-κB signaling pathway activation.
Pulmonary tuberculosisSignal transducer and activator of transcription 1(STAT1)Mac-rophage apoptosisMAPK/NF-κB signaling pathway
NETL
NSTL
万方数据
