Fig 1.
Scheme of synthesis of thiazolidine containing benzothiazole derivatives and structure of synthesized compounds.
Table 1.
Antioxidant activity and IC50 values of the synthesized derivatives.
Fig 2.
Synthesized benzothiazoles possess anti-inflammatory potential and improved histological alterations in carrageenan-induced paw edema A) Anti-inflammatory effect of compounds (3d, 3e) and indomethacin in carrageenan-induced paw edema in mice.
Each bar represents paw volume displacement after 1, 2, 3, 4, and 5h of treatment. The data was analyzed by ANOVA followed by post-hoc Tukey’s test. ###p < 0.001 vs. saline group, **p < 0.01, ***p < 0.001 vs. carrageenan group (n = 6/group), B) Histopathological alterations as shown by H&E staining (10x, scale bar 50µm n = 6/group).
Fig 3.
Ameliorative potential of compound 3d, 3e and indomethacin on inflammatory markers (A) NFκB expression as quantified by ELISA (D) Immunohistochemistry results for p-NFκB expression in mouse paw following edema (B) TNF-α expression in carrageenan treated mice using ELISA (E) immunohistochemistry results for TNF-α in mouse paw following edema (C) COX-2 expression in carrageenan treated mice using ELISA (F) immunohistochemistry results for COX-2 in mouse paw edema.
The data are expressed as mean ± SEM, n = 6/group. ###p < 0.001 vs saline. *p < 0.05 **p < 0.01, ***p < 0.001 vs. carrageenan group. Scale bar 50µm, 10x.
Fig 4.
Compounds 3d and 3e restored antioxidant markers in paw edema (A) GSH, (B) GST, (C) CAT, (D) LPO and (E) SOD in carrageenan-induced paw edema in mice paw tissues.
Values expressed as mean ± SEM. One way ANOVA with post-hoc Tukey’s test. ###p < 0.001 vs, saline group, *p < 0.05, **p< 0.01, ***p < 0.001 vs, carrageenan group. n = 6/group.
Table 2.
Effect of compounds and omeprazole against ethanol-induced ulcer in mice.
Fig 5.
Synthesized benzothiazoles improved mucosal injury and histological damages in ethanol-induced gastric mucosal injury (A) Gross appearance of the gastric mucosa of mice pretreated with (a) saline (10mL/kg), (b) ethanol (1 mL/100g) severe injuries are seen, as ethanol produced excessive necrosis of gastric mucosa, pretreated with (c) 3b (5 mg/kg), (d) 3b (10 mg/kg), (e) 3d (5 mg/kg), (f) 3d (10 mg/kg), (g) 3e (5 mg/kg), (h) 3e (10 mg/kg), (i) omeprazole (20 mg/kg).
(B) Histopathological slides showing the effect of compound 3b, 3d, 3e, and omeprazole in ethanol-treated mice gastric tissues using hematoxylin and eosin staining histopathological technique. Bar 50 µm, magnification 10x. n = 6/group.
Fig 6.
Compounds 3b, 3d, and 3e mitigated inflammatory mediators after gastric mucosal injury (A) NFκB expression as quantified by ELISA (D) Immunohistochemistry results for p-NFκB expression in mouse gastric ulcer (B) TNF-α expression in ethanol-treated mice using ELISA (E) Immunohistochemistry results for TNF-α in mouse gastric ulcer (C) COX-2 expression in ethanol-treated mice using ELISA (F) Immunohistochemistry results for COX-2 in mouse gastric ulcer.
The data are expressed as mean ± SEM, n = 6/group. ###p < 0.001 vs. saline.***p < 0.001, **p < 0.01, *p < 0.05 vs ethanol group. Scale bar 50µm, 10x.
Fig 7.
Treatment groups (3b, 3d, 3e) demonstrated antioxidant potential against oxidative stress (A) GSH, (B) GST, (C) CAT, (D) LPO and (E) SOD in ethanol-induced ulcers in mice stomach tissues.
Values expressed as mean ± SEM (n = 6/group). One-way ANOVA with post-hoc Tukey’s test. ###p < 0.001 vs saline group, *p < 0.05, **p< 0.01, ***p < 0.001 vs ethanol group.
Table 3.
Binding affinities of newly synthesized derivatives.