Effect of electroacupuncture at Lower He-Sea points including Yanglingquan (GB 34) on nuclear factor-κB and interleukin-1β in guinea pigs with acute cholecystitis / 针灸推拿医学（英文版）

ABSTRACT

Objective: To observe the effect of electroacupuncture (EA) at Lower He-Sea points on the expression levels of interleukin-1β (IL-1β) in the serum and gallbladder tissues, and nuclear factor-κB (NF-κB) in gallbladder tissues of the guinea pigs with acute cholecystitis (AC), and to explore whether Yanglingquan (GB 34), the Lower He-Sea point pertaining to Dan Fu (gallbladder), is relatively specific for the Dan Fu (gallbladder) disorders. Methods: Eighty-two healthy guinea pigs were randomly divided into 6 groups according to the random number table method, a blank group, a model group, a Yanglingquan (GB 34) group, a Zusanli (ST 36) group, a Shangjuxu (ST 37) group, and a Xiajuxu (ST 39) group, with 12 guinea pigs in the blank group while 14 in the other groups, respectively, half males and half females in each group. Except for the blank group, guinea pigs in the other groups were injected with E. coli into the gallbladder to establish AC models. Guinea pigs in the blank group were fed routinely without special treatment; those in the model group were daily tied up for 30 min without EA treatment; those in the 4 groups receiving EA treatment were acupunctured at the corresponding Lower He-Sea points after daily binding and stimulated with the SDZ-V EA instrument. After successful modeling and treatment for 5 d, blood was collected from the abdominal aorta of the guinea pigs, and the gallbladder tissues in each group were isolated for hematoxylin-eosin (HE) staining to observe the morphological changes. Enzyme-linked immunosorbent assay (ELISA) was used to detect the serum IL-1β level, and immunohistochemistry (IHC) was used to detect the expression levels of NF-κB and IL-1β in gallbladder. Results: On the 3rd day after modeling, the guinea pigs in the five groups with modeling were mentally depressed with decreased appetite, significantly reduced activities, slouch, lassitude, slack and matted fur, and loose stools; two guinea pigs were selected from each group (one male and one female, not included in the final statistics) to isolate the gallbladder after sacrifice; macroscopic observation showed that the gallbladder wall was differently thickened; the bile color was dark green and opaque with particles suspended or accumulated; light microscope observation showed that the submucosal blood vessels of the gallbladder were congested, along with mucosal edema, ulceration, necrosis, shedding, and a large number of inflammatory cells infiltrating in the lamina propria, indicating that the AC model was successfully prepared. Compared with the model group, the gallbladder tissue injuries of the four groups receiving EA treatment were all differently repaired, the serum IL-1β levels were reduced (P<0.01 or P<0.05), and the IL-1β levels in the gallbladder tissues were reduced (P<0.01 or P<0.05). Compared with the model group, the NF-κB expression level in the Yanglingquan (GB 34) group was significantly reduced (P<0.01), but was not statistical different in the Zusanli (ST 36) group, Shangjuxu (ST 37) group and Xiajuxu (ST 39) group (all P>0.05). Compared with the Yanglingquan (GB 34) group, the gallbladder tissues of the Zusanli (ST 36) group, Shangjuxu (ST 37) group and Xiajuxu (ST 39) group were more severely damaged, and the expression levels of serum IL-1β, the NF-κB and IL-1β in the gallbladder tissues were increased (P<0.01 or P<0.05). Intervention effect of Yanglingquan (GB 34) on AC guinea pigs was superior to that of Zusanli (ST 36), Shangjuxu (ST 37) and Xiajuxu (ST 39). Conclusion: EA at the Lower He-Sea points of the stomach, large intestine, small intestine and gallbladder can produce curative effects on AC guinea pigs and reduced the inflammatory symptoms. Intervention effect of Yanglingquan (GB 34) on AC guinea pigs is superior to that of Zusanli (ST 36), Shangjuxu (ST 37) and Xiajuxu (ST 39). The mechanism of EA at Yanglingquan (GB 34) in treating AC may be regulating IL-1β and NF-κB to control the inflammatory response and improve the gallbladder tissue damage.