{'fraction_non_alphanumeric': 0.04595695171611402, 'fraction_numerical': 0.029086678301337987, 'mean_word_length': 5.254545454545455, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Early renal tubulointerstitial changes and their interventions with Shenkang Injection in diabetic rats].

OBJECTIVE
To explore whether renal tubulointerstitial lesions are early renal pathological changes and its interventions in diabetic rats.


METHODS
The type 2 diabetic rat model was induced by a high-sugar and high-fat diet with a low-dose intraperitoneal injection of streptozotocin. And Shenkang Injection (SKI) was used as an intervention drug. A total of 30 Sprague-Dawley rats were divided randomly into diabetic (DM), DM+SKI (DMSK) and normal control (NC) groups. The general status, blood biochemical parameters, microalbuminuria and urinary N-acetyl-D-glueosaminidas (NAG) were recorded. The insulin resistance of diabetic rats was detected with hyperinsulinemic-euglycemic clamp test.Renal pathological changes were evaluated with periodic acid-Schiff (PAS) staining. The expression of Toll-like receptor 4 (TLR4) in kidney tissue and renal interstitial CD68(+) cells was detected with immunohistochemistry.


RESULTS
The levels of microalbuminuria, urinary NAG, glomerular volume, renal tubular score, TLR4 expression and renal interstitial CD68(+) cells significantly increased in DM rats with body weight loss and insulin resistance (IOD value of TLR4: 6 289.86 ± 272.45 vs 207.14 ± 22.37; CD68(+) cells: 8.79 ± 0.79 vs.1.23 ± 0.52). All changes in DM rats improved after SKI intervention (P < 0.05).


CONCLUSION
Renal tubulointerstitial lesions are early renal damages in type 2 diabetic rats.SKI can attenuate diabetic tubulointerstitial damage and delay the progression of diabetic nephropathy associated with the inhibition of TLR4 expression and inflammation-mediated macrophage infiltration.