Objective: To study the effects of Shuanghuanglian granules on inflammatory factors such as tumor necrosis factor (TNF)-α

interleukin (IL)-6 and nuclear factor (NF)-κB in serum or lung tissues of rats infected with Mycoplasma pneumoniae

so as to further study the pharmacological mechanism of Shuanghuanglian granules. Methods: Mycoplasma pneumoniae pneumonia model in rats was established. Sixty SD rats were randomly divided into the blank control group

the model group

the Shuanghuanglian low

medium

and high dose group and the positive control group. The administration was started after 3 d of continuous infection. After 7 d of continuous administration

serum and lung tissues were collected

and the lung tissues were stained with HE to observe the lesions under an optical microscope. The serum levels of TNF-α and IL-6 were detected by enzyme-linked immunosorbent assay (ELISA). Westernblot was adopted to detect the expression of phosphorylated NF-κB P65 in lung tissues. Results: The serum levels of TNF-α and IL-6 in the blank control group were (0.96±0.23) ng/mL

(451.43±33.42) ng/mL

and the relative content of phosphorylated NF-κB p65 was 0.16±0.05. The lung tissue pathological score of rats in the model group was (4.50±1.32) points

the serum levels of TNF-α and IL-6 were respectively (1.84±0.42) ng/mL and (603.29±63.57) ng/mL

and the relative content of phosphorylated NF-κB p65 was 1.07±0.06

which were higher than those of the blank control group. Serum levels of TNF-α in the Shuanghuanglian low

medium

and high dose group were respectively (1.62±0.32) ng/mL

(1.47±0.31) ng/mL and (1.24±0.25) ng/mL

and serum levels of IL-6 were respectively (551.56±50.93) ng/mL

(509.57±49.92) ng/mL and (487.14±44.15) ng/mL

the relative content of phosphorylated NF-κB p65 were respectively 0.43±0.15

0.12±0.07 and 0.10±0.05

compared with the model group

the dose-dependent decrease was observed. Conclusion: Shuanghuanglian granules can reduce the inflammatory symptoms in the lung tissues by reducing the levels of TNF-α and IL-6

inhibit the abnormal activation of the NF-κB signaling pathway

thereby restoring the normal morphology and physiological functions in lung tissues.